R A Flavell

Summary

Affiliation: Yale University
Country: USA

Publications

  1. pmc Deficiency of small GTPase Rac2 affects T cell activation
    H Yu
    Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
    J Exp Med 194:915-26. 2001
  2. pmc The role of CTCF in regulating nuclear organization
    Adam Williams
    Department of Immunobiology and Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA
    J Exp Med 205:747-50. 2008
  3. pmc Immune recognition of Pseudomonas aeruginosa mediated by the IPAF/NLRC4 inflammasome
    Fayyaz S Sutterwala
    Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
    J Exp Med 204:3235-45. 2007
  4. pmc Gadd45 beta and Gadd45 gamma are critical for regulating autoimmunity
    Lin Liu
    Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA
    J Exp Med 202:1341-7. 2005
  5. pmc The transcription cofactor Hopx is required for regulatory T cell function in dendritic cell-mediated peripheral T cell unresponsiveness
    Daniel Hawiger
    Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA
    Nat Immunol 11:962-8. 2010
  6. pmc Control of TH17 cells occurs in the small intestine
    Enric Esplugues
    Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Nature 475:514-8. 2011
  7. pmc Inflammasome-mediated dysbiosis regulates progression of NAFLD and obesity
    Jorge Henao-Mejia
    Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Nature 482:179-85. 2012
  8. pmc Defective survival of naive CD8+ T lymphocytes in the absence of the beta3 regulatory subunit of voltage-gated calcium channels
    Mithilesh K Jha
    Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA
    Nat Immunol 10:1275-82. 2009
  9. pmc IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine
    Samuel Huber
    Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Nature 491:259-63. 2012
  10. pmc Innate instruction of adaptive immunity revisited: the inflammasome
    Stephanie C Eisenbarth
    Department of Laboratory Medicine, Yale University School of Medicine, New Haven, CT 06520, USA
    EMBO Mol Med 1:92-8. 2009

Research Grants

  1. Vaccine responsiveness to Borrelia burgdorferi OspA
    Richard Flavell; Fiscal Year: 2006
  2. The Role of IL-2 in Autoimmune Diabetes
    Richard Flavell; Fiscal Year: 2006
  3. Dys/Regulation of the Immune System in Autoimmunity
    Richard Flavell; Fiscal Year: 2006
  4. Roles of Nod2 in the Pathogenesis of Crohn's Disease
    Richard Flavell; Fiscal Year: 2006
  5. Vaccine responsiveness to Borrelia burgdorferi OspA
    Richard Flavell; Fiscal Year: 2007
  6. The Role of IL-2 in Autoimmune Diabetes
    Richard Flavell; Fiscal Year: 2007
  7. Roles of Nod2 in the Pathogenesis of Crohn's Disease
    Richard Flavell; Fiscal Year: 2007
  8. PATHOGENESIS AND PREVENTION OF AUTOIMMUNE DIABETES
    Richard Flavell; Fiscal Year: 2007
  9. The role of Bcl-Rambo in thymic involution
    Richard Flavell; Fiscal Year: 2009
  10. PATHOGENESIS AND PREVENTION OF AUTOIMMUNE DIABETES
    Richard Flavell; Fiscal Year: 2009

Collaborators

Detail Information

Publications155 found, 100 shown here

  1. pmc Deficiency of small GTPase Rac2 affects T cell activation
    H Yu
    Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
    J Exp Med 194:915-26. 2001
    ..The phenotypic similarity of Rac2(-/-) to Vav(-/-) cells implicates Rac2 as a downstream mediator of Vav signaling...
  2. pmc The role of CTCF in regulating nuclear organization
    Adam Williams
    Department of Immunobiology and Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA
    J Exp Med 205:747-50. 2008
    ..New data now help define how CTCF mediates both long-range intrachromosomal and interchromosomal interactions, and highlight CTCF as an important factor in determining the three-dimensional structure of the genome...
  3. pmc Immune recognition of Pseudomonas aeruginosa mediated by the IPAF/NLRC4 inflammasome
    Fayyaz S Sutterwala
    Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
    J Exp Med 204:3235-45. 2007
    ..This study shows a key role for IPAF and capase-1 in innate immune responses to the pathogen P. aeruginosa, and also demonstrates that virulent ExoU-expressing strains of P. aeruginosa can circumvent this innate immune response...
  4. pmc Gadd45 beta and Gadd45 gamma are critical for regulating autoimmunity
    Lin Liu
    Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA
    J Exp Med 202:1341-7. 2005
    ..Our findings therefore identify the Gadd45beta/Gadd45gamma-mediated control of effector autoimmune lymphocytes as an attractive novel target for autoimmune disease therapy...
  5. pmc The transcription cofactor Hopx is required for regulatory T cell function in dendritic cell-mediated peripheral T cell unresponsiveness
    Daniel Hawiger
    Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA
    Nat Immunol 11:962-8. 2010
    ..Thus, Hopx is required for the function of T(reg) cells induced by DCs and the promotion of DC-mediated T cell unresponsiveness in vivo...
  6. pmc Control of TH17 cells occurs in the small intestine
    Enric Esplugues
    Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Nature 475:514-8. 2011
    ..These results identify mechanisms limiting T(H)17 cell pathogenicity and implicate the gastrointestinal tract as a site for control of T(H)17 cells...
  7. pmc Inflammasome-mediated dysbiosis regulates progression of NAFLD and obesity
    Jorge Henao-Mejia
    Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Nature 482:179-85. 2012
    ....
  8. pmc Defective survival of naive CD8+ T lymphocytes in the absence of the beta3 regulatory subunit of voltage-gated calcium channels
    Mithilesh K Jha
    Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA
    Nat Immunol 10:1275-82. 2009
    ..Ca(v)1.4 and beta3 associated with T cell signaling machinery and Ca(v)1.4 localized in lipid rafts. Our data demonstrate a mechanism by which Ca(2+) entry is controlled by a Ca(v)1.4-beta3 channel complex in T cells...
  9. pmc IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine
    Samuel Huber
    Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Nature 491:259-63. 2012
    ..Thus, the IL-22-IL-22BP axis critically regulates intestinal tissue repair and tumorigenesis in the colon...
  10. pmc Innate instruction of adaptive immunity revisited: the inflammasome
    Stephanie C Eisenbarth
    Department of Laboratory Medicine, Yale University School of Medicine, New Haven, CT 06520, USA
    EMBO Mol Med 1:92-8. 2009
    ..Basic questions in our understanding of Nlrp3 inflammasome activation are also presented...
  11. pmc Memory/effector (CD45RB(lo)) CD4 T cells are controlled directly by IL-10 and cause IL-22-dependent intestinal pathology
    Masahito Kamanaka
    Department of Immunobiology, School of Medicine, Yale University, New Haven, CT 06520, USA
    J Exp Med 208:1027-40. 2011
    ..Our results highlight characteristic differences between colitis induced by naive (CD45RB(hi)) and memory/effector (T(reg) cell-depleted CD45RB(lo)) cells and different ways that IL-22 impacts inflammatory bowel disease...
  12. doi request reprint Inflammasomes and metabolic disease
    Jorge Henao-Mejia
    Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520 email
    Annu Rev Physiol 76:57-78. 2014
    ..Here, we review recent evidence that highlights inflammasomes as critical sensors of metabolic perturbations in multiple tissues and their role in the progression of highly prevalent metabolic diseases. ..
  13. pmc Inflammasome activation mediates inflammation and outcome in humans and mice with pneumococcal meningitis
    Madelijn Geldhoff
    Department of Neurology, Center of Infection and Immunity Amsterdam CINIMA, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
    BMC Infect Dis 13:358. 2013
    ..In a murine model of pneumococcal meningitis we examined the pathophysiological roles of two inflammasome proteins, NLRP3 (Nod-like receptor protein-3) and adaptor protein ASC (apoptosis-associated speck-like protein)...
  14. pmc LoxP-FRT Trap (LOFT): a simple and flexible system for conventional and reversible gene targeting
    Barbara H Chaiyachati
    Department of Immunobiology, Yale University Medical School, 300 Cedar Street, New Haven, CT 06520, USA
    BMC Biol 10:96. 2013
    ..However, a major limitation of this method is that gene KO is not reversible. A number of methods have been developed to overcome this, but each method has its own limitations...
  15. pmc IL-10 signaling in CD4+ T cells is critical for the pathogenesis of collagen-induced arthritis
    Jian Tao
    Section of Rheumatology, Department of Internal Medicine, Yale School of Medicine, 333 Cedar Street, New Haven, CT 06520 8031, USA
    Arthritis Res Ther 13:R212. 2011
    ..However, the role of this cytokine in T cells in the pathogenesis of collagen-induced arthritis is unclear. The purpose of this study was to define the role of IL-10 signaling in T cells in the pathogenesis of collagen-induced arthritis...
  16. pmc Long-term activation of TLR3 by poly(I:C) induces inflammation and impairs lung function in mice
    Nicole C Stowell
    Discovery Research, Centocor Research and Development, Inc, Radnor, Pennsylvania, USA
    Respir Res 10:43. 2009
    ..Thus, an understanding of TLR3 activation should provide insight into the mechanisms underlying virus-induced exacerbations of pulmonary diseases...
  17. pmc Prostaglandin F2alpha- and FAS-activating antibody-induced regression of the corpus luteum involves caspase-8 and is defective in caspase-3 deficient mice
    Silvia F Carambula
    Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital Harvard Medical School, Boston, Massachusetts 02114, USA
    Reprod Biol Endocrinol 1:15. 2003
    ....
  18. pmc Innate recognition of non-self nucleic acids
    Hongbo Chi
    Department of Immunology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Genome Biol 9:211. 2008
    ..Here we discuss the recognition of and responses to non-self nucleic acids via these receptors as well as their involvement in autoimmune diseases...
  19. pmc Plexin-B1 plays a redundant role during mouse development and in tumour angiogenesis
    Pietro Fazzari
    Institute for Cancer Research and Treatment, University of Torino Medical School, Division of Molecular Oncology, Candiolo, Turin, Italy
    BMC Dev Biol 7:55. 2007
    ..In order to shed light on PlexinB1 function in vivo, we therefore undertook the genomic targeting of the mouse gene to obtain loss of function mutants...
  20. pmc The polarization of immune cells in the tumour environment by TGFbeta
    Richard A Flavell
    Yale University School of Medicine, 300 Cedar Street, TAC S 569, PO Box 208011, New Haven, Connecticut 06520, USA
    Nat Rev Immunol 10:554-67. 2010
    ..An overview of the current drugs and reagents available for inhibiting TGFbeta-induced signalling and their phase in clinical development is also provided...
  21. ncbi request reprint Overexpression of IL-7R alpha provides a competitive advantage during early T-cell development
    Yasmina Laouar
    Section of Immunobiology, Yale University School of Medicine, 300 Ceda St, CAB S 569, New Haven, CT 06520, USA
    Blood 103:1985-94. 2004
    ..This advantage occurred at early stages of T-cell development. Our findings support the model that overexpression of growth factor receptors can contribute to proliferation and malignancy...
  22. ncbi request reprint Signaling and cell death in lymphocytes
    R A Flavell
    Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520 8011, USA
    Inflamm Res 51:80-2. 2002
    ..Here we discuss transcription factors and signaling pathways that are selectively expressed or activated in Th1 and Th2 cells to regulate cytokine gene expression, cell proliferation and apoptosis...
  23. pmc Neonatal tumor necrosis factor alpha promotes diabetes in nonobese diabetic mice by CD154-independent antigen presentation to CD8(+) T cells
    E A Green
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Exp Med 191:225-38. 2000
    ..These data provide new insights into the mechanisms by which inflammatory stimuli can bypass CD154-CD40 immune regulatory signals and cause activation of autoreactive T cells...
  24. ncbi request reprint Pancreatic infiltration but not diabetes occurs in the relative absence of MHC class II-restricted CD4 T cells: studies using NOD/CIITA-deficient mice
    C Mora
    Section of Immunobiology, Yale University School of Medicine, Howard Hughes Medical Institute, New Haven, CT 06520, USA
    J Immunol 162:4576-88. 1999
    ..This highlights the fact that a high number of in vitro activated autoaggressive CD8 T cells can over-ride the requirement for CD4 T cell help for the onset of diabetes...
  25. ncbi request reprint JNK1 is required for T cell-mediated immunity against Leishmania major infection
    S L Constant
    Section of Immunobiology, Yale University School of Medicine, and Howard Hughes Medical Institute New Haven, CT 06520, USA
    J Immunol 165:2671-6. 2000
    ..These findings demonstrate that the negative regulation of Th2 cytokine production by the JNK1 signaling pathway is essential for generating Th1-polarized immunity against intracellular pathogens, such as Leishmania major...
  26. ncbi request reprint GADD45gamma mediates the activation of the p38 and JNK MAP kinase pathways and cytokine production in effector TH1 cells
    B Lu
    Section of Immunobiology and, Yale University School of Medicine, 310 Cedar Street, New Haven, CT 06520, USA
    Immunity 14:583-90. 2001
    ..Additionally, GADD45gamma deficiencies caused reduced contact hypersensitivity in mice. Thus, GADD45gamma mediates activation of the p38 and JNK pathways and effector function of TH1 cells...
  27. ncbi request reprint The Jnk1 and Jnk2 protein kinases are required for regional specific apoptosis during early brain development
    C Y Kuan
    Section of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Neuron 22:667-76. 1999
    ..In contrast, increased apoptosis and caspase activation were found in the mutant forebrain, leading to precocious degeneration. These results suggest that Jnk1 and Jnk2 regulate region-specific apoptosis during early brain development...
  28. ncbi request reprint JNK is required for effector T-cell function but not for T-cell activation
    C Dong
    Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Nature 405:91-4. 2000
    ..However, production of effector T-cell cytokines did require JNK. Thus, JNK is necessary for T-cell differentiation but not for naive T-cell activation...
  29. ncbi request reprint Defective T cell differentiation in the absence of Jnk1
    C Dong
    Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA
    Science 282:2092-5. 1998
    ..Thus, the JNK1 signaling pathway plays a key role in T cell receptor-initiated TH cell proliferation, apoptosis, and differentiation...
  30. ncbi request reprint CD62L is required on effector cells for local interactions in the CNS to cause myelin damage in experimental allergic encephalomyelitis
    I S Grewal
    Department of Immunology, Genentech Incorporated, South San Francisco, CA 94080, USA
    Immunity 14:291-302. 2001
    ....
  31. pmc Regulation of IL-4 expression by the transcription factor JunB during T helper cell differentiation
    B Li
    Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine, New Haven CT 06520, USA
    EMBO J 18:420-32. 1999
    ..Thus, the early increase of JunB protein in Th2 cells can provide the specificity for c-Maf in IL-4 expression during T cell development and directs thereby Th2 differentiation...
  32. ncbi request reprint Role of the guanosine triphosphatase Rac2 in T helper 1 cell differentiation
    B Li
    Section of Immunobiology and Howard Hughes Medical Institute, Yale University School of Medicine, 310 Cedar Street, New Haven, CT 06520 8011, USA
    Science 288:2219-22. 2000
    ..Moreover, T cells from Rac2-/- mice showed decreased IFN-gamma production under TH1 conditions in vitro. Thus, Rac2 activates TH1-specific signaling and IFN-gamma gene expression...
  33. ncbi request reprint Deficiency in caspase-9 or caspase-3 induces compensatory caspase activation
    T S Zheng
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Nat Med 6:1241-7. 2000
    ..Our findings provide direct experimental evidence for compensatory pathways of caspase activation. This issue should therefore be considered in developing caspase inhibitors for therapeutic applications...
  34. pmc Defective IL-12 production in mitogen-activated protein (MAP) kinase kinase 3 (Mkk3)-deficient mice
    H T Lu
    Howard Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
    EMBO J 18:1845-57. 1999
    ..We conclude that the p38 MAP kinase, activated through MKK3, is required for the production of inflammatory cytokines by both antigen-presenting cells and CD4(+) T cells...
  35. ncbi request reprint Disruption of the murine MRP (multidrug resistance protein) gene leads to increased sensitivity to etoposide (VP-16) and increased levels of glutathione
    A Lorico
    Department of Pharmacology, Cancer Center, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Cancer Res 57:5238-42. 1997
    ..The findings demonstrate that mrp is dispensable for development and growth but exerts a role in drug detoxification and GSH metabolism...
  36. pmc Lymph node germinal centers form in the absence of follicular dendritic cell networks
    P A Koni
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520 8011, USA
    J Exp Med 189:855-64. 1999
    ....
  37. ncbi request reprint ICOS co-stimulatory receptor is essential for T-cell activation and function
    C Dong
    Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Nature 409:97-101. 2001
    ..ICOS-/- mice showed greatly enhanced susceptibility to experimental autoimmune encephalomyelitis, indicating that ICOS has a protective role in inflammatory autoimmune diseases...
  38. ncbi request reprint Differentiation of CD4+ T cells to Th1 cells requires MAP kinase JNK2
    D D Yang
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Immunity 9:575-85. 1998
    ..The JNK MAP kinase signaling pathway, therefore, plays an important role in the balance of Th1 and Th2 immune responses...
  39. ncbi request reprint Local expression of TNFalpha in neonatal NOD mice promotes diabetes by enhancing presentation of islet antigens
    E A Green
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Immunity 9:733-43. 1998
    ..Thus, inflammation can trigger autoimmunity by recruiting and activating dendritic cells/macrophages to present self-antigens to autoreactive T cells...
  40. ncbi request reprint The role of Fas in autoimmune diabetes
    A V Chervonsky
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Cell 89:17-24. 1997
    ..Thus, induction of Fas expression on beta cells and their subsequent destruction constitutes the main pathogenic mechanism in autoimmune diabetes...
  41. ncbi request reprint Signaling by the JNK group of MAP kinases. c-jun N-terminal Kinase
    C Dong
    Section of Immunobiology, Yale University School of Medicine and Howard Hughes, Medical Institute, New Haven, Connecticut 06520, USA
    J Clin Immunol 21:253-7. 2001
    ..In this review, we summarize these advances in understanding the expression, function, and regulation of the JNK pathway in T-lymphocyte activation and differentiation...
  42. ncbi request reprint Defective antigen processing in GILT-free mice
    M Maric
    Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA
    Science 294:1361-5. 2001
    ..The response to hen egg lysozyme, a model antigen with a compact structure containing four disulfide bonds, was examined in detail...
  43. ncbi request reprint Targeted expression of the anti-apoptotic gene CrmA to NOD pancreatic islets protects from autoimmune diabetes
    I Millet
    Department of Internal Medicine and Immunobiology, Section of Endocrinology, Yale University School of Medicine, P O Box 208020, 333 Cedar Street, TAC S141, New Haven, CT 06520, USA
    J Autoimmun 26:7-15. 2006
    ..We conclude that anti-apoptotic genes such as CrmA might be potential candidates to enhance islet graft survival in T1DM...
  44. ncbi request reprint Autoimmune lpr/lpr mice deficient in CD40 ligand: spontaneous Ig class switching with dichotomy of autoantibody responses
    J Ma
    Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520 8031, USA
    J Immunol 157:417-26. 1996
    ..They also suggest that different mechanisms may be responsible for eliciting autoantibody responses in lpr/lpr mice...
  45. ncbi request reprint Lymphotoxin-beta-deficient mice show defective antiviral immunity
    D P Berger
    Department of Neuropharmacology, Division of Virology, IMM 6, Department of Immunology, IMM 25, The Scripps Research Institute, 10550 N Torrey Pines Road, La Jolla, California, 92037, USA
    Virology 260:136-47. 1999
    ..These data indicate that the absence of LTbeta does not affect the intrinsic function of T lymphocytes or of dendritic cells but that the structural integrity of the spleen is strongly associated with generation of antiviral immunity...
  46. ncbi request reprint Carrier-mediated enhancement of cognate T cell help: the basis for enhanced immunogenicity of meningococcal outer membrane protein polysaccharide conjugate vaccine
    M Perez-Melgosa
    Department of Immunology, University of Washington, Seattle, 98195, USA
    Eur J Immunol 31:2373-81. 2001
    ..Neither porins nor lipopolysaccharide fully reproduced the effects of OMPC. These studies indicate that OMPC acts both as carrier and adjuvant, and thereby enhances T cell-dependent antibody responses in human infants...
  47. pmc Invariant chain controls H2-M proteolysis in mouse splenocytes and dendritic cells
    P Pierre
    Department of Cell Biology and Section of Immunobiology, Ludwig Institute for Cancer Research, Yale University School of Medicine, New Haven, CT 06520 8002, USA
    J Exp Med 191:1057-62. 2000
    ..Thus, Ii chain may act as a lysosomal protease inhibitor in B cells and DCs, with its deletion contributing indirectly to the loss of H2-M...
  48. ncbi request reprint Requirement for CD40 ligand in costimulation induction, T cell activation, and experimental allergic encephalomyelitis
    I S Grewal
    Howard Hughes Medical Institute, and Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA
    Science 273:1864-7. 1996
    ..1(+) antigen-presenting cells (APCs). Thus, CD40L is required to induce costimulatory activity on APCs for in vivo activation of CD4(+) T cells to produce IFN-gamma and to evoke autoimmunity...
  49. ncbi request reprint Role of CD4+ T cells in pathogenesis associated with Leishmania amazonensis infection
    L Soong
    Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, CT 06520, USA
    J Immunol 158:5374-83. 1997
    ..amazonensis and Leishmania major suggest that these parasites may have adapted different strategies regarding the CD4-dependent immune response...
  50. ncbi request reprint alpha beta T cell regulation and CD40 ligand dependence in murine systemic autoimmunity
    S L Peng
    Section of Rheumatology, Yale University School of Medicine, New Haven, CT 06510, USA
    J Immunol 158:2464-70. 1997
    ..Thus, both alpha beta and non-alpha beta T cells, such as gamma delta T cells, regulate systemic autoimmunity by CD40L-dependent and -independent mechanisms...
  51. ncbi request reprint Borrelia burgdorferi-infected, interleukin-6-deficient mice have decreased Th2 responses and increased lyme arthritis
    J Anguita
    Section of Rheumatology, Department of Internal Medicine, Howard Hughes Medical Institute, New Haven, Connecticut, USA
    J Infect Dis 178:1512-5. 1998
    ..These results extend previous in vitro observations by demonstrating an in vivo role for IL-6 in the differentiation of CD4 T cells toward a Th2 phenotype and further show that CD4 T cell responses influence murine Lyme arthritis...
  52. ncbi request reprint Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene
    D D Yang
    Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Nature 389:865-70. 1997
    ..These data indicate that the observed neuroprotection is due to the extinction of a Jnk3-mediated signalling pathway, which is an important component in the pathogenesis of glutamate neurotoxicity...
  53. ncbi request reprint Cutting edge: critical role of inducible costimulator in germinal center reactions
    C Dong
    Section of Immunobiology, Yale University School of Medicine and Howard Hughes Medical Institute, New Haven, CT 06514, USA
    J Immunol 166:3659-62. 2001
    ..Remarkably, GC formation in response to a secondary recall challenge was completely absent in ICOS knockout mice. These data establish a critical role of ICOS in regulation of humoral immunity...
  54. ncbi request reprint Distinct effects of Jak3 signaling on alphabeta and gammadelta thymocyte development
    E E Eynon
    Section of Immunobiology and Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA
    J Immunol 162:1448-59. 1999
    ..The results also emphasize the fundamentally different requirements for differentiation of the alphabeta and gammadelta T cell lineages...
  55. pmc Impaired primary T cell responses in L-selectin-deficient mice
    J Xu
    Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Exp Med 183:589-98. 1996
    ..L-selectin does not appear to be rate limiting for the events leading to antigen-driven neutrophil recruitment, since normal DTH responses are obtained at late time points after immunization...
  56. ncbi request reprint Mice lacking the MHC class II transactivator (CIITA) show tissue-specific impairment of MHC class II expression
    C H Chang
    Howard Hughes Medical Institute, Yale School of Medicine, New Haven, Connecticut 06510, USA
    Immunity 4:167-78. 1996
    ..Consequently, CIITA(-/-) mice are impaired in T-dependent antigen responses and MHC class II-mediated allogeneic responses...
  57. pmc Human exposure to a granulocytic Ehrlichia and other tick-borne agents in Connecticut
    L A Magnarelli
    Department of Entomology, The Connecticut Agricultural Experiment Station, New Haven, Connecticut 06504, USA
    J Clin Microbiol 36:2823-7. 1998
    ..1%) of 180 patients had antibodies to two or more tick-borne agents. Therefore, when one of these diseases is clinically suspected or diagnosed, clinicians should consider the possibility of other current or past tick-borne infections...
  58. ncbi request reprint NF-kappa B activation by the pre-T cell receptor serves as a selective survival signal in T lymphocyte development
    R E Voll
    Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
    Immunity 13:677-89. 2000
    ..Therefore, signals emanating from the pre-TCR are mediated at least in part by NF-kappa B, which provides a selective survival signal for developing thymocytes with productive beta chain rearrangements...
  59. pmc Widespread expression of an autoantigen-GAD65 transgene does not tolerize non-obese diabetic mice and can exacerbate disease
    L Geng
    Department of Molecular Cellular and Developmental Biology, Yale University Kline Biology Tower 219 Prospect Street, New Haven, CT 06520, USA
    Proc Natl Acad Sci U S A 95:10055-60. 1998
    ....
  60. ncbi request reprint Requirement for invariant chain in B cell maturation and function
    I Shachar
    Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA
    Science 274:106-8. 1996
    ..This block was independent of major histocompatability complex class II expression and was an intrinsic feature of B cells that correlated with the amount of Ii. Thus, Ii participates by an unknown mechanism in B cell maturation...
  61. ncbi request reprint Impairment of antigen-specific T-cell priming in mice lacking CD40 ligand
    I S Grewal
    Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Nature 378:617-20. 1995
    ....
  62. pmc A role for tumor necrosis factor receptor type 1 in gut-associated lymphoid tissue development: genetic evidence of synergism with lymphotoxin beta
    P A Koni
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Exp Med 187:1977-83. 1998
    ..A complete lack of only PPs in mice heterozygous for both ltalpha and ltbeta, but not ltalpha or ltbeta alone, suggests a similar two-ligand phenomenon in PP development and may explain the incomplete lack of PPs seen in tnfr1-/- mice...
  63. ncbi request reprint Mice deficient for the CD40 ligand
    J Xu
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510
    Immunity 1:423-31. 1994
    ..In summary, our study confirms the important role of CD40-CD40L interactions in thymus-dependent humoral immune responses and germinal center formation...
  64. ncbi request reprint Recognition of double-stranded RNA and activation of NF-kappaB by Toll-like receptor 3
    L Alexopoulou
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, 06520, USA
    Nature 413:732-8. 2001
    ..Moreover, poly(I:C) can induce activation of NF-kappaB and mitogen-activated protein (MAP) kinases independently of MyD88, and cause dendritic cells to mature...
  65. ncbi request reprint Targeted expression of the neuropeptide calcitonin gene-related peptide to beta cells prevents diabetes in NOD mice
    A Khachatryan
    Yale University School of Medicine, Department of Orthopaedics and Rehabilitation, New Haven, CT 06510, USA
    J Immunol 158:1409-16. 1997
    ..These data also suggest that endogenous CGRP concentrated in sensory nerve endings may regulate locally the immune response, further strengthening the importance of the functional neuroimmune link...
  66. ncbi request reprint Disruption of CD40-CD40 ligand interactions results in an enhanced susceptibility to Leishmania amazonensis infection
    L Soong
    Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut 06520 8011, USA
    Immunity 4:263-73. 1996
    ..These results indicate an essential role of cognate CD40-CD40L interactions in the generation of cellular immune responses against an intracellular parasite...
  67. pmc T-cell responsiveness to an oncogenic peripheral protein and spontaneous autoimmunity in transgenic mice
    T Geiger
    Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06510
    Proc Natl Acad Sci U S A 89:2985-9. 1992
    ..This result argues that T cells may become spontaneously autoreactive to certain postnatally expressed peripheral proteins and that this reactivity may lead to autoimmune disease...
  68. ncbi request reprint The role of cell death in regulating the size and shape of the mammalian forebrain
    T F Haydar
    Section of Neurobiology, Yale University School of Medicine, New Haven, CT 06510, USA
    Cereb Cortex 9:621-6. 1999
    ..Thus, the precise coordination of different apoptotic signaling pathways during early stages of neurogenesis is crucial for regulation of the proper cortical size and shape...
  69. ncbi request reprint Immune-mediated eradication of tumors through the blockade of transforming growth factor-beta signaling in T cells
    L Gorelik
    Section of Immunobiology, Yale University School of Medicine and Howard Hughes Medical Institute, New Haven, Connecticut, USA
    Nat Med 7:1118-22. 2001
    ..Our data indicate that T-cell-specific blockade of TGF-beta signaling has strong therapeutic potential to shift the balance of the immune response in favor of anti-tumor immunity...
  70. pmc Regulation of AP-1 and NFAT transcription factors during thymic selection of T cells
    M Rincon
    Section of Immunobiology, Yale University, School of Medicine, New Haven, Connecticut 06510, USA
    Mol Cell Biol 16:1074-84. 1996
    ..This could be a mechanism to prevent the activation of DP thymocytes before selection has taken place...
  71. ncbi request reprint Walking through the forest of transgenic models of human disease
    E E Eynon
    Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut, USA
    Immunol Rev 169:5-10. 1999
    ..Second, expression of individual molecules can be altered in the context of established disease models. We describe here some of the models in use as well as the limitations and promise of this research...
  72. ncbi request reprint Regulation of IL-4 gene expression by distal regulatory elements and GATA-3 at the chromatin level
    G R Lee
    Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
    Immunity 14:447-59. 2001
    ..GATA-3 mediated strong enhancement of IL-4 promoter activity in Th1 cells when the promoter was embedded in the minilocus or linked to HSS and IE, demonstrating that GATA-3 acts through these elements to regulate IL-4 gene expression...
  73. ncbi request reprint A self-augmenting gene expression cassette for enhanced and sustained transgene expression in the presence of proinflammatory cytokines
    P Luo
    Department of Immunology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    DNA Cell Biol 25:659-67. 2006
    ..Our data demonstrate that the self-augmenting strategy provides a promising approach to achieve high and sustained transgene expression in vivo...
  74. ncbi request reprint Distinct roles in lymphoid organogenesis for lymphotoxins alpha and beta revealed in lymphotoxin beta-deficient mice
    P A Koni
    Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Immunity 6:491-500. 1997
    ....
  75. ncbi request reprint Caspase knockouts: matters of life and death
    T S Zheng
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Cell Death Differ 6:1043-53. 1999
    ..We will also provide our prediction on the direction of future studies in this ever-growing field of caspases...
  76. pmc The invariant chain is required for intracellular transport and function of major histocompatibility complex class II molecules
    E A Elliott
    Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510
    J Exp Med 179:681-94. 1994
    ..Thus, although alpha and beta chains can fold and form dimers on their own, the absence of Ii chain causes them to be recognized as "misfolded" and retained in the same compartments as bona fide misfolded proteins...
  77. ncbi request reprint The molecular basis of T cell differentiation
    R A Flavell
    Yale University School of Medicine, Howard Hughes Medical Institute, New Haven, CT 06520 8011, USA
    Immunol Res 19:159-68. 1999
    ..Understanding these mechanisms is likely to lead in the long-term to ways to intervene in these processes and, therefore, to direct immune response in therapeutically useful directions...
  78. ncbi request reprint Protective antibodies develop, and murine Lyme arthritis regresses, in the absence of MHC class II and CD4+ T cells
    E Fikrig
    Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA
    J Immunol 159:5682-6. 1997
    ..17 SCID mice. These data suggest that CD4+ T cells and MHC class II-mediated responses are not required for the generation of protective Abs or the regression of arthritis, but may be important in the resolution of Lyme carditis in mice...
  79. ncbi request reprint Neural tube, skeletal and body wall defects in mice lacking transcription factor AP-2
    J Zhang
    Department of Biology, Yale University, New Haven, Connecticut 06511, USA
    Nature 381:238-41. 1996
    ..Analysis of these mice earlier in embryogenesis indicates a failure of cranial neural-tube closure and defects in cranial ganglia development. We have shown that AP-2 is a fundamental regulator of mammalian craniofacial development...
  80. pmc Serologic diagnosis of Lyme borreliosis by using enzyme-linked immunosorbent assays with recombinant antigens
    L A Magnarelli
    Department of Entomology, The Connecticut Agricultural Experiment Station, New Haven, Connecticut 06504, USA
    J Clin Microbiol 38:1735-9. 2000
    ....
  81. ncbi request reprint Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice
    K Kuida
    Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Nature 384:368-72. 1996
    ..Thus CPP32 is shown to play a critical role during morphogenetic cell death in the mammalian brain...
  82. ncbi request reprint The relationship of inflammation and initiation of autoimmune disease: role of TNF super family members
    R A Flavell
    Section of Immunobiology, Yale University School of Medicine, Howard Hughes Medical Institute, New Haven, CT, USA
    Curr Top Microbiol Immunol 266:1-9. 2002
  83. pmc Caspase-3 controls both cytoplasmic and nuclear events associated with Fas-mediated apoptosis in vivo
    T S Zheng
    Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
    Proc Natl Acad Sci U S A 95:13618-23. 1998
    ..The altered cleavage of these key substrates is likely responsible for the aberrant apoptosis observed in both hepatocytes and thymocytes deficient in caspase-3...
  84. pmc Follicular dendritic cells and dissemination of Creutzfeldt-Jakob disease
    L Manuelidis
    Section of Neuropathology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Virol 74:8614-22. 2000
    ..While it is still not clear where the infectious agent replicates, macrophages can sequester appreciable levels of infectivity and hence act as reservoirs for prolonged latent infection...
  85. ncbi request reprint B7 costimulation is necessary for the activation of the lytic function in cytotoxic T lymphocyte precursors
    S Guerder
    Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
    J Immunol 155:5167-74. 1995
    ..The production of IFN-gamma by CD8 T cells, however, does not appear to require costimulation...
  86. ncbi request reprint Disruption of cytokine signaling in lymphoid development: unique contributions of the common cytokine gamma chain and the Jak3 kinase
    E E Eynon
    Section of Immunobiology, Yale University School of Medicine, New Haven, CT, USA
    J Interferon Cytokine Res 16:677-84. 1996
  87. ncbi request reprint Essential role of phosphoinositide metabolism in synaptic vesicle recycling
    O Cremona
    Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Cell 99:179-88. 1999
    ..These results provide genetic evidence for a crucial role of phosphoinositide metabolism in synaptic vesicle recycling...
  88. ncbi request reprint Reconstitution of invariant chain function in transgenic mice in vivo by individual p31 and p41 isoforms
    I Shachar
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Immunity 3:373-83. 1995
    ..Furthermore, p31 and p41 retrieve the CD4+ T cell population, which is reduced in the (delta Ii) mice. Moreover, the immune response to protein antigen is restored by both isoforms...
  89. ncbi request reprint Expression of the co-stimulator molecule B7-1 in pancreatic beta-cells accelerates diabetes in the NOD mouse
    S Wong
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520 8011
    Diabetes 44:326-9. 1995
    ..This illustrates that B7-1 is a very potent co-stimulatory molecule in vivo and that its presence on the surface of tissue cells can potentiate the autoimmune process...
  90. pmc Human CD4 restores normal T cell development and function in mice deficient in murine CD4
    Y M Law
    Section of Immunobiology, Howard Hughes Medical Institute, School of Medicine, Yale University, New Haven, Connecticut 06510
    J Exp Med 179:1233-42. 1994
    ....
  91. ncbi request reprint Altered cytokine export and apoptosis in mice deficient in interleukin-1 beta converting enzyme
    K Kuida
    Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06510, USA
    Science 267:2000-3. 1995
    ..Despite this defect in apoptosis, ICE-/- mice proceed normally through development...
  92. ncbi request reprint Direct physical interaction involving CD40 ligand on T cells and CD40 on B cells is required to propagate MMTV
    A V Chervonsky
    Section of Immunobiology, Yale University School of Medicine, Howard Hughes Medical Institute, New Haven, Connecticut 06510, USA
    Immunity 3:139-46. 1995
    ..The initial step in SAG-dependent T cell activation, and hence the MMTV life cycle, may be mediated by non-B cells, because splenocytes from B cell-deficient SAG-transgenic mice are able to activate cognate T cells...
  93. ncbi request reprint Crucial role for the Nalp3 inflammasome in the immunostimulatory properties of aluminium adjuvants
    Stephanie C Eisenbarth
    Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Nature 453:1122-6. 2008
    ..This is likely to affect how we design effective, but safe, adjuvants in the future...
  94. ncbi request reprint Transforming growth factor-beta and the immune response: implications for anticancer therapy
    Stephen H Wrzesinski
    Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA
    Clin Cancer Res 13:5262-70. 2007
    ....
  95. pmc Direct regulation of Gata3 expression determines the T helper differentiation potential of Notch
    Derk Amsen
    Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
    Immunity 27:89-99. 2007
    ..Moreover, absence of GATA-3 turned Notch from a Th2 inducer into a powerful inducer of Th1 differentiation. Therefore, Gata3 is a critical element determining inductive Th2 differentiation and limiting Th1 differentiation by Notch...
  96. ncbi request reprint T cell-produced transforming growth factor-beta1 controls T cell tolerance and regulates Th1- and Th17-cell differentiation
    Ming O Li
    Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
    Immunity 26:579-91. 2007
    ..These findings reveal essential roles for T cell-produced TGF-beta1 in controlling differentiation of T helper cells and controlling inflammatory diseases...
  97. pmc Regulatory role of B cells in a murine model of allergic airway disease
    Anurag Singh
    Department of Immunology, University of Connecticut Health Center, Framington, CT 06030, USA
    J Immunol 180:7318-26. 2008
    ..These findings illustrated a novel regulatory role for regional B cells in AAD and suggested a possible contributory role of B cells, along with other cell types, in the establishment of LIT...
  98. ncbi request reprint Transforming growth factor-beta controls development, homeostasis, and tolerance of T cells by regulatory T cell-dependent and -independent mechanisms
    Ming O Li
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Immunity 25:455-71. 2006
    ..This study reveals pleiotropic functions of TGF-beta signaling in T cells that may ensure a diverse and self-tolerant T cell repertoire in vivo...

Research Grants33

  1. Vaccine responsiveness to Borrelia burgdorferi OspA
    Richard Flavell; Fiscal Year: 2006
    ..abstract_text> ..
  2. The Role of IL-2 in Autoimmune Diabetes
    Richard Flavell; Fiscal Year: 2006
    ..We will utilize our IL-2 knock-in mice to test these two mutually nonexclusive hypotheses. ..
  3. Dys/Regulation of the Immune System in Autoimmunity
    Richard Flavell; Fiscal Year: 2006
    ..The program is coordinated by frequent meetings of the program faculty and research workers bringing together these diverse approaches to address a common goal. ..
  4. Roles of Nod2 in the Pathogenesis of Crohn's Disease
    Richard Flavell; Fiscal Year: 2006
    ..Furthermore, by using mice in which Rip2, the kinase downstream of Nod2, is deficient, we will try to reveal if the IBD pathology caused by Nod2 mutation is dependent on Rip2. ..
  5. Vaccine responsiveness to Borrelia burgdorferi OspA
    Richard Flavell; Fiscal Year: 2007
    ..abstract_text> ..
  6. The Role of IL-2 in Autoimmune Diabetes
    Richard Flavell; Fiscal Year: 2007
    ..We will utilize our IL-2 knock-in mice to test these two mutually nonexclusive hypotheses. ..
  7. Roles of Nod2 in the Pathogenesis of Crohn's Disease
    Richard Flavell; Fiscal Year: 2007
    ..Furthermore, by using mice in which Rip2, the kinase downstream of Nod2, is deficient, we will try to reveal if the IBD pathology caused by Nod2 mutation is dependent on Rip2. ..
  8. PATHOGENESIS AND PREVENTION OF AUTOIMMUNE DIABETES
    Richard Flavell; Fiscal Year: 2007
    ..We will determine whether TGF-beta is instrumental in this process and we will elucidate the mechanism whereby this occurs. ..
  9. The role of Bcl-Rambo in thymic involution
    Richard Flavell; Fiscal Year: 2009
    ....
  10. PATHOGENESIS AND PREVENTION OF AUTOIMMUNE DIABETES
    Richard Flavell; Fiscal Year: 2009
    ..We will determine whether TGF-beta is instrumental in this process and we will elucidate the mechanism whereby this occurs. ..
  11. The role of Bcl-Rambo in thymic involution
    Richard A Flavell; Fiscal Year: 2010
    ....
  12. PATHOGENESIS AND PREVENTION OF AUTOIMMUNE DIABETES
    Richard A Flavell; Fiscal Year: 2010
    ..We will determine whether TGF-beta is instrumental in this process and we will elucidate the mechanism whereby this occurs. ..
  13. Immunoregulatory Mechanisms in Autoimmune Diabetes
    Richard Flavell; Fiscal Year: 2005
    ..We will use regulated expression of TGF beta in the islets and a new T cell transgene which renders T cells resistant to inhibition to TGF beta to ask how TGF beta blocks IDDM and what happens in conditions when it cannot act. ..
  14. Roles of Nod2 in the Pathogenesis of Crohn's Disease
    Richard Flavell; Fiscal Year: 2005
    ..Furthermore, by using mice in which Rip2, the kinase downstream of Nod2, is deficient, we will try to reveal if the IBD pathology caused by Nod2 mutation is dependent on Rip2. ..
  15. The Role of IL-2 in Autoimmune Diabetes
    Richard Flavell; Fiscal Year: 2005
    ..We will utilize our IL-2 knock-in mice to test these two mutually nonexclusive hypotheses. ..
  16. PATHOGENESIS AND PREVENTION OF AUTOIMMUNE DIABETES
    Richard Flavell; Fiscal Year: 1999
    ..Finally, they will determine whether TNF expression initiating early in the life of the NOD mouse, protects or exacerbates from disease, and, if exacerbation is observed, they will determine the mechanism by which that occurs. ..
  17. PATHOGENESIS AND PREVENTION OF AUTOIMMUNE DIABETES
    Richard Flavell; Fiscal Year: 2000
    ..Finally, they will determine whether TNF expression initiating early in the life of the NOD mouse, protects or exacerbates from disease, and, if exacerbation is observed, they will determine the mechanism by which that occurs. ..
  18. Immunoregulatory Mechanisms in Autoimmune Diabetes
    Richard Flavell; Fiscal Year: 2001
    ..We will use regulated expression of TGF beta in the islets and a new T cell transgene which renders T cells resistant to inhibition to TGF beta to ask how TGF beta blocks IDDM and what happens in conditions when it cannot act. ..
  19. Immunoregulatory Mechanisms in Autoimmune Diabetes
    Richard Flavell; Fiscal Year: 2002
    ..We will use regulated expression of TGF beta in the islets and a new T cell transgene which renders T cells resistant to inhibition to TGF beta to ask how TGF beta blocks IDDM and what happens in conditions when it cannot act. ..
  20. IL-2 in Autoimmune Diabetes
    Richard Flavell; Fiscal Year: 2003
    ..We will utilize our IL-2 knock-in mice to test these two mutually nonexclusive hypotheses. ..
  21. Immunoregulatory Mechanisms in Autoimmune Diabetes
    Richard Flavell; Fiscal Year: 2003
    ..We will use regulated expression of TGF beta in the islets and a new T cell transgene which renders T cells resistant to inhibition to TGF beta to ask how TGF beta blocks IDDM and what happens in conditions when it cannot act. ..
  22. Vaccine responsiveness to Borrelia burgdorferi OspA
    Richard Flavell; Fiscal Year: 2003
    ..abstract_text> ..
  23. The Role of IL-2 in Autoimmune Diabetes
    Richard Flavell; Fiscal Year: 2004
    ..We will utilize our IL-2 knock-in mice to test these two mutually nonexclusive hypotheses. ..
  24. Immunoregulatory Mechanisms in Autoimmune Diabetes
    Richard Flavell; Fiscal Year: 2004
    ..We will use regulated expression of TGF beta in the islets and a new T cell transgene which renders T cells resistant to inhibition to TGF beta to ask how TGF beta blocks IDDM and what happens in conditions when it cannot act. ..
  25. Roles of Nod2 in the Pathogenesis of Crohn's Disease
    Richard Flavell; Fiscal Year: 2004
    ..Furthermore, by using mice in which Rip2, the kinase downstream of Nod2, is deficient, we will try to reveal if the IBD pathology caused by Nod2 mutation is dependent on Rip2. ..
  26. Understanding Hemotopoietic Neoplasias using Humanized Mice
    MARKUS GABRIEL MANZ; Fiscal Year: 2010
    ..This model will serve as a platform for preclinical testing of medicines against cancer with a better likelihood of how well these medicines will work in people. ..