W Strober

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi Regulation of experimental mucosal inflammation
    W Strober
    Mucosal Immunity Section, Laboratory of Clinical Investigation, NIAID, National Institute of Health, Bethesda, Maryland 20892 1890, USA
    Acta Odontol Scand 59:244-7. 2001
  2. ncbi The immunology of mucosal models of inflammation
    Warren Strober
    Mucosal Immunity Section, Laboratory of Clinical Investigation, NIAID, NIH, Bethesda, Maryland 20892 1890, USA
    Annu Rev Immunol 20:495-549. 2002
  3. ncbi GATA-3 suppresses Th1 development by downregulation of Stat4 and not through effects on IL-12Rbeta2 chain or T-bet
    Takashi Usui
    Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892, USA
    Immunity 18:415-28. 2003
  4. ncbi Downstream effector functions of T-cell activation
    Warren Strober
    National Institutes of Health, Bethesda, Maryland, USA
    J Pediatr Gastroenterol Nutr 40:S26. 2005
  5. ncbi Signalling pathways and molecular interactions of NOD1 and NOD2
    Warren Strober
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10 CRC, 5W3940, 10 Center Drive, Bethesda, Maryland 20892, USA
    Nat Rev Immunol 6:9-20. 2006
  6. ncbi Immunology. Unraveling gut inflammation
    Warren Strober
    Laboratory of Host Defenses, National Institutes of Health. Bethesda, MD 20892-1890. USA
    Science 313:1052-4. 2006
  7. ncbi Insights into the mechanism of oral tolerance derived from the study of models of mucosal inflammation
    Warren Strober
    The Mucosal Immunity Section, Laboratory of Host Defense, NIAID, National Institutes of Health, Bethesda, MD 20892, USA
    Ann N Y Acad Sci 1029:115-31. 2004
  8. ncbi The fundamental basis of inflammatory bowel disease
    Warren Strober
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA
    J Clin Invest 117:514-21. 2007
  9. ncbi NOD2, an intracellular innate immune sensor involved in host defense and Crohn's disease
    W Strober
    Laboratory of Host Defenses, Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA
    Mucosal Immunol 4:484-95. 2011
  10. ncbi The LTi cell, an immunologic chameleon
    Warren Strober
    NIH NIAID, Bethesda, MD 20892, USA
    Immunity 33:650-2. 2010

Collaborators

Detail Information

Publications105 found, 100 shown here

  1. ncbi Regulation of experimental mucosal inflammation
    W Strober
    Mucosal Immunity Section, Laboratory of Clinical Investigation, NIAID, National Institute of Health, Bethesda, Maryland 20892 1890, USA
    Acta Odontol Scand 59:244-7. 2001
    ..These and other developments in the understanding of inflammation paint a bright future for cytokine-based therapeutic agents. It is now apparent that these therapies are not only effective and safe but also potentially long-lasting...
  2. ncbi The immunology of mucosal models of inflammation
    Warren Strober
    Mucosal Immunity Section, Laboratory of Clinical Investigation, NIAID, NIH, Bethesda, Maryland 20892 1890, USA
    Annu Rev Immunol 20:495-549. 2002
    ..What emerges is that murine models of mucosal inflammation have given us a road map that allows us to begin to define the immunology of the IBDs in all its complexity and to find unexpected ways to treat these diseases...
  3. ncbi GATA-3 suppresses Th1 development by downregulation of Stat4 and not through effects on IL-12Rbeta2 chain or T-bet
    Takashi Usui
    Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892, USA
    Immunity 18:415-28. 2003
    ..These findings reassert that Stat4 signaling is a central element of Th1/Th2 development...
  4. ncbi Downstream effector functions of T-cell activation
    Warren Strober
    National Institutes of Health, Bethesda, Maryland, USA
    J Pediatr Gastroenterol Nutr 40:S26. 2005
  5. ncbi Signalling pathways and molecular interactions of NOD1 and NOD2
    Warren Strober
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10 CRC, 5W3940, 10 Center Drive, Bethesda, Maryland 20892, USA
    Nat Rev Immunol 6:9-20. 2006
    ....
  6. ncbi Immunology. Unraveling gut inflammation
    Warren Strober
    Laboratory of Host Defenses, National Institutes of Health. Bethesda, MD 20892-1890. USA
    Science 313:1052-4. 2006
  7. ncbi Insights into the mechanism of oral tolerance derived from the study of models of mucosal inflammation
    Warren Strober
    The Mucosal Immunity Section, Laboratory of Host Defense, NIAID, National Institutes of Health, Bethesda, MD 20892, USA
    Ann N Y Acad Sci 1029:115-31. 2004
    ....
  8. ncbi The fundamental basis of inflammatory bowel disease
    Warren Strober
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA
    J Clin Invest 117:514-21. 2007
    ..Here we examine these hypotheses and conclude that IBD is indeed characterized by an abnormal mucosal immune response but that microbial factors and epithelial cell abnormalities can facilitate this response...
  9. ncbi NOD2, an intracellular innate immune sensor involved in host defense and Crohn's disease
    W Strober
    Laboratory of Host Defenses, Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA
    Mucosal Immunol 4:484-95. 2011
    ..host disease. In this review, we summarize recent findings regarding normal functions of NOD2 and discuss the mechanisms by which NOD2 polymorphisms associated with Crohn's disease lead to intestinal inflammation...
  10. ncbi The LTi cell, an immunologic chameleon
    Warren Strober
    NIH NIAID, Bethesda, MD 20892, USA
    Immunity 33:650-2. 2010
    ..In this issue of Immunity, Vonarbourg et. al. (2010) describe how these cells assume several different guises, each associated with different LTi functions...
  11. ncbi Vitamin A rewrites the ABCs of oral tolerance
    W Strober
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA
    Mucosal Immunol 1:92-5. 2008
    ..Thus, we arrive at the somewhat surprising realization that mucosal unresponsiveness is, appropriately enough, related to the availability of a factor in the food stream...
  12. ncbi Proinflammatory cytokines in the pathogenesis of inflammatory bowel diseases
    Warren Strober
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Gastroenterology 140:1756-67. 2011
    ..In this review, we will explore this cytokine landscape with the view of providing an understanding of how recent and future anticytokine therapies actually function...
  13. ncbi Adherent-invasive E. coli in Crohn disease: bacterial "agent provocateur"
    Warren Strober
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland, USA
    J Clin Invest 121:841-4. 2011
    ..These findings provide a mechanism of AIEC penetration but do not prove that AIEC is causing a primary infection in the Peyer's patches that is necessary for the initiation or persistence of CD inflammation...
  14. ncbi The molecular basis of NOD2 susceptibility mutations in Crohn's disease
    W Strober
    Mucosal Immunity Section, Laboratory of Host Defenses, NIAID, NIH, Bethesda, Maryland, USA
    Mucosal Immunol 1:S5-9. 2008
    ..The finding that MDP administration prevents experimental colitis opens the door to the possibility that such treatment might quell Crohn's disease relapses in patients without NOD2 abnormalities...
  15. ncbi The multifaceted influence of the mucosal microflora on mucosal dendritic cell responses
    Warren Strober
    Mucosal Immunity Section, Laboratory of Host Defenses, NIAID, NIH Bethesda, MD, USA
    Immunity 31:377-88. 2009
    ....
  16. ncbi Proinflammatory cytokines underlying the inflammation of Crohn's disease
    Warren Strober
    Mucosal Immunity Section, Laboratory of Host Defenses, NIAID, Bethesda, Maryland 20892 6612, USA
    Curr Opin Gastroenterol 26:310-7. 2010
    ....
  17. ncbi Role of IL-12 in intrathymic negative selection
    B R Ludviksson
    Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA
    J Immunol 163:4349-59. 1999
    ....
  18. ncbi Induction and prevention of colonic inflammation in IL-2-deficient mice
    R O Ehrhardt
    Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 158:566-73. 1997
    ..These findings suggest that in the absence of IL-2 systemic administration of Ag induces primarily Th1 cells driven by overexpression of heterodimeric IL-12...
  19. ncbi Administration of mAb against alpha E beta 7 prevents and ameliorates immunization-induced colitis in IL-2-/- mice
    B R Ludviksson
    Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA
    J Immunol 162:4975-82. 1999
    ..Thus, the above findings demonstrate that the onset and maintenance of inflammatory bowel disease depends on the colonic localization of lamina propria CD4+ lymphocytes expressing alpha E beta 7...
  20. ncbi Activated STAT4 has an essential role in Th1 differentiation and proliferation that is independent of its role in the maintenance of IL-12R beta 2 chain expression and signaling
    Ryuta Nishikomori
    Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases NIH, Bethesda, MD 20892, USA
    J Immunol 169:4388-98. 2002
    ..This implies that STAT4 is an essential element in the early events of Th1 differentiation...
  21. ncbi Cell contact-dependent immunosuppression by CD4(+)CD25(+) regulatory T cells is mediated by cell surface-bound transforming growth factor beta
    K Nakamura
    Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Exp Med 194:629-44. 2001
    ..This, plus the fact that we could find no evidence that a soluble factor mediates suppression, strongly suggests that CD4(+)CD25(+) T cells exert immunosuppression by a cell-cell interaction involving cell surface TGF-beta1...
  22. ncbi Interleukin-12 production by dendritic cells. The role of CD40-CD40L interactions in Th1 T-cell responses
    B L Kelsall
    Mucosal Immunity Section, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Ann N Y Acad Sci 795:116-26. 1996
    ....
  23. ncbi Defects of monocyte interleukin 12 production and humoral immunity in Whipple's disease
    T Marth
    Mucosal Immunity Section, National Institutes of Health, Bethesda, Maryland, USA
    Gastroenterology 113:442-8. 1997
    ..The aim of this study was to test whether this macrophage dysfunction is the cause or result of previously shown T-cell defects...
  24. ncbi BALB/c mice bearing a transgenic IL-12 receptor beta 2 gene exhibit a nonhealing phenotype to Leishmania major infection despite intact IL-12 signaling
    R Nishikomori
    Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 166:6776-83. 2001
    ..major infection...
  25. ncbi T-bet regulates Th1 responses through essential effects on GATA-3 function rather than on IFNG gene acetylation and transcription
    Takashi Usui
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Disease NIAID, National Institutes of Health NIH, Bethesda, MD 20892, USA
    J Exp Med 203:755-66. 2006
    ..Thus, the principal function of T-bet in developing Th1 cells is to negatively regulate GATA-3 rather than to positively regulate the IFNG gene...
  26. ncbi A novel lymphoproliferative/autoimmune syndrome resembling murine lpr/gld disease
    M C Sneller
    Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892
    J Clin Invest 90:334-41. 1992
    ..The clinical and immunological features of this syndrome resemble the lymphoproliferative/autoimmune disease seen in lpr and gld mice...
  27. ncbi TGF-beta production regulates the development of the 2,4,6-trinitrophenol-conjugated keyhole limpet hemocyanin-induced colonic inflammation in IL-2-deficient mice
    B R Ludviksson
    Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA
    J Immunol 159:3622-8. 1997
    ....
  28. ncbi Active Wegener's granulomatosis is associated with HLA-DR+ CD4+ T cells exhibiting an unbalanced Th1-type T cell cytokine pattern: reversal with IL-10
    B R Ludviksson
    Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA
    J Immunol 160:3602-9. 1998
    ..These data suggest that T cells from WG patients overproduce IFN-gamma and TNF-alpha, probably due to dysregulated IL-12 secretion, and that IL-10 may therefore have therapeutic implications for this disease...
  29. ncbi Clincal, immunologic, and genetic features of an autoimmune lymphoproliferative syndrome associated with abnormal lymphocyte apoptosis
    M C Sneller
    Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Blood 89:1341-8. 1997
    ..Fas gene mutations account for impaired lymphocyte apoptosis in only a subset of patients with ALPS...
  30. ncbi Distinct populations of dendritic cells are present in the subepithelial dome and T cell regions of the murine Peyer's patch
    B L Kelsall
    Mucosal Immunity Section, National Institutes for Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 22908, USA
    J Exp Med 183:237-47. 1996
    ....
  31. ncbi Increases in circulating and lymphoid tissue interleukin-10 in autoimmune lymphoproliferative syndrome are associated with disease expression
    U Lopatin
    Laboratory of Clinical Investigation, Clinical Research Training Program, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA
    Blood 97:3161-70. 2001
    ..Nonetheless, in vitro studies showed no influence of IL-10 on the survival of CD4(-)CD8(-) T cells. Overexpression of IL-10 in patients with inherited apoptotic defects is strongly associated with the overt manifestations of ALPS...
  32. ncbi Cross-linking of OX40 ligand, a member of the TNF/NGF cytokine family, induces proliferation and differentiation in murine splenic B cells
    E Stuber
    Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Immunity 2:507-21. 1995
    ..This effect may thus be one mechanism for OX40-induced increase in immunoglobulin secretion. In conclusion, our data suggest that the OX40-OX40L interaction is a novel pathway in T cell-dependent B cell proliferation and differentiation...
  33. ncbi The interrelated roles of TGF-beta and IL-10 in the regulation of experimental colitis
    Ivan J Fuss
    Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 168:900-8. 2002
    ..Therefore, these studies suggest that TGF-beta production is a primary mechanism of counter-regulation of Th1 T cell-mediated mucosal inflammation, and that IL-10 is necessary as a secondary factor that facilitates TGF-beta production...
  34. ncbi IL-13 signaling through the IL-13alpha2 receptor is involved in induction of TGF-beta1 production and fibrosis
    Stefan Fichtner-Feigl
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10 CRC 5W3864, 10 Center Drive, Bethesda, Maryland 20892, USA
    Nat Med 12:99-106. 2006
    ..These data suggest that IL-13Ralpha(2) signaling during prolonged inflammation is an important therapeutic target for the prevention of TGF-beta(1)-mediated fibrosis...
  35. ncbi Dysregulated intrathymic development in the IL-2-deficient mouse leads to colitis-inducing thymocytes
    B R Ludviksson
    Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 158:104-11. 1997
    ..Taken together, these data indicate that, in the absence of IL-2, thymocyte maturation is abnormally directed by IL-12 toward the generation of mature, activated Th1-type thymocytes that are capable of mediating colitis...
  36. ncbi Factors involved in the differentiation of TGF-beta-producing cells from naive CD4+ T cells: IL-4 and IFN-gamma have opposing effects, while TGF-beta positively regulates its own production
    R A Seder
    Lymphokine Regulation Unit, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 160:5719-28. 1998
    ..Finally, the addition of exogenous TGF-beta to priming cultures significantly enhanced the production of TGF-beta upon restimulation, demonstrating that TGF-beta has a role in self-regulating its own production...
  37. ncbi An inherited disorder of lymphocyte apoptosis: the autoimmune lymphoproliferative syndrome
    S E Straus
    Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1888, USA
    Ann Intern Med 130:591-601. 1999
    ..Defective apoptosis may also contribute to a heightened risk for lymphoma...
  38. ncbi Reciprocal IFN-gamma and TGF-beta responses regulate the occurrence of mucosal inflammation
    W Strober
    Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA
    Immunol Today 18:61-4. 1997
    ..Interventions that artificially bring the excessive Th1-cell response back into balance, such as administration of IL-12 antagonists, should therefore find a central place in the treatment of the disease...
  39. ncbi Specific missense mutations in NEMO result in hyper-IgM syndrome with hypohydrotic ectodermal dysplasia
    A Jain
    Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA
    Nat Immunol 2:223-8. 2001
    ....
  40. ncbi TGF-beta 1 plays an important role in the mechanism of CD4+CD25+ regulatory T cell activity in both humans and mice
    Kazuhiko Nakamura
    Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11N238, 10 Center Drive, Bethesda, MD 20892, USA
    J Immunol 172:834-42. 2004
    ..Together, these studies demonstrate that TGF-beta1 produced by CD4+CD25+ T cells is involved in the suppressor activity of these cells, particularly in their ability to regulate intestinal inflammation...
  41. ncbi Oxazolone colitis, a Th2 colitis model resembling ulcerative colitis, is mediated by IL-13-producing NK-T cells
    Frank Heller
    Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Immunity 17:629-38. 2002
    ..These data thus describe a cellular mechanism underlying an experimental colitis that may explain the pathogenesis of ulcerative colitis...
  42. ncbi Nucleotide binding oligomerization domain 2 deficiency leads to dysregulated TLR2 signaling and induction of antigen-specific colitis
    Tomohiro Watanabe
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10 CRC, Room 5W3940, 10 Center Drive, Bethesda, Maryland 20892, USA
    Immunity 25:473-85. 2006
    ..Thus, NOD2-deficient mice become susceptible to colitis as a result of increased TLR2 responses when they have the capacity to respond to an antigen expressed by mucosal bacteria...
  43. ncbi Muramyl dipeptide activation of nucleotide-binding oligomerization domain 2 protects mice from experimental colitis
    Tomohiro Watanabe
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland 20892, USA
    J Clin Invest 118:545-59. 2008
    ....
  44. ncbi NOD2 transgenic mice exhibit enhanced MDP-mediated down-regulation of TLR2 responses and resistance to colitis induction
    Zhiqiong Yang
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA
    Gastroenterology 133:1510-21. 2007
    ..Mutations in the CARD15 gene encoding NOD2 are susceptibility factors in Crohn's disease. We explored the mechanism of this susceptibility using mice that over express NOD2...
  45. ncbi Induction of IL-13 triggers TGF-beta1-dependent tissue fibrosis in chronic 2,4,6-trinitrobenzene sulfonic acid colitis
    Stefan Fichtner-Feigl
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 178:5859-70. 2007
    ..A similar mechanism may obtain in certain forms of human inflammatory bowel disease...
  46. ncbi Disparate CD4+ lamina propria (LP) lymphokine secretion profiles in inflammatory bowel disease. Crohn's disease LP cells manifest increased secretion of IFN-gamma, whereas ulcerative colitis LP cells manifest increased secretion of IL-5
    I J Fuss
    Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 157:1261-70. 1996
    ..These different patterns may determine the type of inflammatory process present...
  47. ncbi The immunological and genetic basis of inflammatory bowel disease
    Gerd Bouma
    The Mucosal Immunity Section, National Institutes of Health, Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institutes of Allergy and Infectious Diseases, 10 Center Drive, Room 11N238, Bethesda, Maryland 20892, USA
    Nat Rev Immunol 3:521-33. 2003
    ..Here, we discuss these recent findings and the implications for therapy...
  48. ncbi Transforming growth factor (TGF)-beta1-producing regulatory T cells induce Smad-mediated interleukin 10 secretion that facilitates coordinated immunoregulatory activity and amelioration of TGF-beta1-mediated fibrosis
    Atsushi Kitani
    National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11N238, 10 Center Drive, Bethesda, MD 20892, USA
    J Exp Med 198:1179-88. 2003
    ..Taken together, these findings suggest that the induction of IL-10 by TGF-beta1 is not fortuitous, but instead fulfills important requirements of TGF-beta1 function after its secretion by regulatory T cells...
  49. ncbi Wright-Giemsa and nonspecific esterase staining of cells
    W Strober
    National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA
    Curr Protoc Cytom . 2001
    ..Thus, this staining reaction can be used to identify monocytes/macrophages in cell preparations...
  50. ncbi NOD2 regulation of Toll-like receptor responses and the pathogenesis of Crohn's disease
    T Watanabe
    National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10 CRC, 10 Center Drive, Bethesda, MD 20892, USA
    Gut 54:1515-8. 2005
  51. ncbi Successful granulocyte-colony stimulating factor treatment of Crohn's disease is associated with the appearance of circulating interleukin-10-producing T cells and increased lamina propria plasmacytoid dendritic cells
    P J Mannon
    Mucosal Immunity Section, Laboratory of Host Defense, NIAID, NIH, Bethesda, MD, USA
    Clin Exp Immunol 155:447-56. 2009
    ....
  52. ncbi The TNF-family cytokine TL1A drives IL-13-dependent small intestinal inflammation
    F Meylan
    Immunoregulation Section, Autoimmunity Branch, NIAMS, Bethesda, Maryland, USA
    Mucosal Immunol 4:172-85. 2011
    ..These results establish a novel link between TL1A and interleukin 13 (IL-13) responses that results in small intestinal inflammation, and also establish that TL1A-DR3 interactions are necessary and sufficient for T cell-dependent IBD...
  53. ncbi Mucosal AIDS vaccine reduces disease and viral load in gut reservoir and blood after mucosal infection of macaques
    I M Belyakov
    Molecular Immunogenetics and Vaccine Research Section, Metabolism Branch, National Cancer Institute, Bethesda, Maryland, USA
    Nat Med 7:1320-6. 2001
    ..Moreover, CD4+ T cells were better preserved. Thus, induction of CTLs in the intestinal mucosa, a key site of virus replication, with a mucosal AIDS vaccine ameliorates infection by SHIV in non-human primates...
  54. ncbi Cutting edge: regulatory T cells induce CD4+CD25-Foxp3- T cells or are self-induced to become Th17 cells in the absence of exogenous TGF-beta
    Lili Xu
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 178:6725-9. 2007
    ..They thus have important implications to our understanding of regulatory T cell function and their possible therapeutic use...
  55. ncbi NOD2 is a negative regulator of Toll-like receptor 2-mediated T helper type 1 responses
    Tomohiro Watanabe
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10 Room 11N238, 10 Center Drive, Bethesda, Maryland 20892, USA
    Nat Immunol 5:800-8. 2004
    ..Thus, CARD15 mutations may lead to disease by causing excessive T(H)1 responses...
  56. ncbi Treatment of murine Th1- and Th2-mediated inflammatory bowel disease with NF-kappa B decoy oligonucleotides
    Stefan Fichtner-Feigl
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland 20892, USA
    J Clin Invest 115:3057-71. 2005
    ..In each case, decoy administration led to inflammation-clearing effects, suggesting a therapeutic potency applicable to human IBD...
  57. ncbi Both mucosal and systemic routes of immunization with the live, attenuated NYVAC/simian immunodeficiency virus SIV(gpe) recombinant vaccine result in gag-specific CD8(+) T-cell responses in mucosal tissues of macaques
    Liljana Stevceva
    Basic Research Laboratory, National Cancer Institute, Bethesda, Maryland 20892, USA
    J Virol 76:11659-76. 2002
    ..We conclude that immunization with a live vector vaccine results in the appearance of CD8(+) T-cell responses at mucosal sites even when the vaccine is delivered by nonmucosal routes...
  58. ncbi A mutation in the Nlrp3 gene causing inflammasome hyperactivation potentiates Th17 cell-dominant immune responses
    Guangxun Meng
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Immunity 30:860-74. 2009
    ..These results demonstrate that the NLRP3 mutation leads to inflammasome hyperactivation and consequently Th17 cell-dominant immunopathology in autoinflammation...
  59. ncbi Mucosal vaccination overcomes the barrier to recombinant vaccinia immunization caused by preexisting poxvirus immunity
    I M Belyakov
    Molecular Immunogenetics and Vaccine Research Section, Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 96:4512-7. 1999
    ..This approach to circumvent previous vaccinia immunity may be useful for induction of protective immunity against infectious diseases and cancer in the sizable populations with preexisting immunity to vaccinia from smallpox vaccination...
  60. ncbi Pax5 (BSAP) regulates the murine immunoglobulin 3' alpha enhancer by suppressing binding of NF-alpha P, a protein that controls heavy chain transcription
    M F Neurath
    Mucosal Immunity Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892 1890, USA
    Proc Natl Acad Sci U S A 92:5336-40. 1995
    ..Pax5 thus regulates the 3' alpha enhancer and immunoglobulin gene transcription by blocking activation by NF-alpha P...
  61. ncbi Molecular mechanisms regulating TGF-beta-induced Foxp3 expression
    L Xu
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA
    Mucosal Immunol 3:230-8. 2010
    ..In this review we discuss these mechanisms, with the aim of presenting a broad picture of how the various observations fit together to form an integrated regulatory regime...
  62. ncbi Effect of transforming growth factor (TGF)-beta 1 on IgA isotype expression. TGF-beta 1 induces a small increase in sIgA+ B cells regardless of the method of B cell activation
    R O Ehrhardt
    Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892
    J Immunol 148:3830-6. 1992
    ..These results are most consistent with the view that TGF-beta provides only a partial or incomplete IgA switch signal but that additional factors are involved in IgA isotype switching and differentiation...
  63. ncbi Interactions between epithelial cells and immune cells in the intestine
    W Strober
    Mucosal Immunity Section, NIAID, NIH, Bethesda, Maryland 20892, USA
    Ann N Y Acad Sci 859:37-45. 1998
    ..Different microorganisms also elicit different response patterns. The information presented provides a basis for a new view of epithelial cell function in relation to host defense...
  64. ncbi Antibodies to complement receptor 3 treat established inflammation in murine models of colitis and a novel model of psoriasiform dermatitis
    Francisco Leon
    Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institute of Health, Bethesda, MD 20892, USA
    J Immunol 177:6974-82. 2006
    ..Administration of anti-CR3 may be a useful therapeutic approach to consider for the treatment of inflammatory bowel disease and psoriasis in humans...
  65. ncbi STAT4 serine phosphorylation is critical for IL-12-induced IFN-gamma production but not for cell proliferation
    Akio Morinobu
    Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal, and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 99:12281-6. 2002
    ..We conclude that phosphorylation of STAT4 on both tyrosine and serine residues is important in promoting normal T(H)1 differentiation and IFN-gamma secretion...
  66. ncbi T-cell-expressed proprotein convertase furin is essential for maintenance of peripheral immune tolerance
    Marko Pesu
    Molecular Immunology and Inflammation Branch, National Institute for Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nature 455:246-50. 2008
    ..Targeting furin has emerged as a strategy in malignant and infectious disease. Our results suggest that inhibiting furin might activate immune responses, but may result in a breakdown in peripheral tolerance...
  67. ncbi Experimental murine colitis is regulated by two genetic loci, including one on chromosome 11 that regulates IL-12 responses
    Gerd Bouma
    Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Gastroenterology 123:554-65. 2002
    ..Immunogenetic analysis of experimental colitis may contribute to the further unraveling of the complex genetic basis of the inflammatory bowel diseases, Crohn's disease and ulcerative colitis...
  68. ncbi Excess IL-12 but not IL-23 accompanies the inflammatory bowel disease associated with common variable immunodeficiency
    Peter J Mannon
    Mucosal Immunity Section, Laboratory of Host Defense, NIAID, NIH, Bethesda, Maryland 20892, USA
    Gastroenterology 131:748-56. 2006
    ..This study was designed to assess the status of the gastrointestinal tract and to define the mucosal immune abnormalities in patients with and without symptomatic gut inflammatory disease...
  69. ncbi Nonclassical CD1d-restricted NK T cells that produce IL-13 characterize an atypical Th2 response in ulcerative colitis
    Ivan J Fuss
    Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda Maryland 20892, USA
    J Clin Invest 113:1490-7. 2004
    ..These studies show that UC is associated with an atypical Th2 response mediated by nonclassical NKT cells producing IL-13 and having cytotoxic potential for epithelial cells...
  70. ncbi National Institutes of Health Center for Human Immunology Conference, September 2009
    Robert B Nussenblatt
    Laboratory of Immunology, National Eye Institute, Maryland 20892, USA
    Ann N Y Acad Sci 1200:E1-23. 2010
    ..The human immunology meeting was held in the Clinical Center of the National Institutes of Health, Bethesda, Maryland, on September 3 and 4, 2009...
  71. ncbi Innate and adaptive immune correlates of vaccine and adjuvant-induced control of mucosal transmission of SIV in macaques
    Yongjun Sui
    Vaccine Branch, Biostatistics and Data Management Section, and Laboratory of Experimental Immunology, National Cancer Institute, and Laboratory of Host Defenses and Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 107:9843-8. 2010
    ..Thus, strategic use of molecular adjuvants can provide better mucosal protection through induction of both innate and adaptive immunity...
  72. ncbi Both IL-12p70 and IL-23 are synthesized during active Crohn's disease and are down-regulated by treatment with anti-IL-12 p40 monoclonal antibody
    Ivan J Fuss
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Inflamm Bowel Dis 12:9-15. 2006
    ..These molecules contain an identical p40 chain that is bound to a p35 chain in IL-12 and a p19 chain in IL-23, making both potentially susceptible to modulation by an anti-IL-12p40 monoclonal antibody (mAb)...
  73. ncbi Impact of vaccine-induced mucosal high-avidity CD8+ CTLs in delay of AIDS viral dissemination from mucosa
    Igor M Belyakov
    Vaccine Branch, National Cancer Institute, Bethesda, MD 20892, USA
    Blood 107:3258-64. 2006
    ....
  74. ncbi Anti-interleukin-12 antibody for active Crohn's disease
    Peter J Mannon
    Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    N Engl J Med 351:2069-79. 2004
    ..Crohn's disease is associated with excess cytokine activity mediated by type 1 helper T (Th1) cells. Interleukin-12 is a key cytokine that initiates Th1-mediated inflammatory responses...
  75. ncbi Cytokines mediating the induction of chronic colitis and colitis-associated fibrosis
    S Fichtner-Feigl
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA
    Mucosal Immunol 1:S24-7. 2008
    ..These studies show that in chronic TNBS colitis, fibrosis is dependent on the development of an IL-13 response that acts through a novel cell-surface-expressed IL-13 receptor to induce TGF-beta(1)...
  76. ncbi A TaqI polymorphism in the 3'UTR of the IL-12 p40 gene correlates with increased IL-12 secretion
    D Seegers
    The Mucosal Immunity Section, National Institutes of Health, Bethesda, MD, USA
    Genes Immun 3:419-23. 2002
    ..While this polymorphism does not appear to be correlated with susceptibility to CD in the limited population of patients tested here, it could influence the occurrence of the disease in certain subsets of patients...
  77. ncbi Impairment of Gag-specific CD8(+) T-cell function in mucosal and systemic compartments of simian immunodeficiency virus mac251- and simian-human immunodeficiency virus KU2-infected macaques
    Z Hel
    Basic Research Laboratory, Bethesda, Maryland 20892, USA
    J Virol 75:11483-95. 2001
    ..The data obtained in this pilot study lead to the hypothesis that disease progression may be associated with loss of virus-specific CD8(+) T-cell function...
  78. ncbi Recent advances in the understanding of the induction and regulation of mucosal inflammation
    Warren Strober
    Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA
    J Gastroenterol 38:55-8. 2003
  79. ncbi Interactions among the transcription factors Runx1, RORgammat and Foxp3 regulate the differentiation of interleukin 17-producing T cells
    Fuping Zhang
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Immunol 9:1297-306. 2008
    ..Thus, our data support a model in which the differential association of Runx1 with Foxp3 and with RORgammat regulates T(H)-17 differentiation...
  80. ncbi The role of IL-13 and NK T cells in experimental and human ulcerative colitis
    I J Fuss
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institutes of Health, Bethesda, Maryland, USA
    Mucosal Immunol 1:S31-3. 2008
    ..In the following review the insights gained from both animal models and human studies as to the function that IL-13 and NK T cells have in the pathogenesis of UC will be discussed...
  81. ncbi Dominant interfering Fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome
    G H Fisher
    Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892 4470, USA
    Cell 81:935-46. 1995
    ..The occurrence of Fas mutations together with abnormal T cell apoptosis in ALPS patients suggests an involvement of Fas in this recently recognized disorder of lymphocyte homeostasis and peripheral self-tolerance...
  82. ncbi Positive and negative transcriptional regulation of the Foxp3 gene is mediated by access and binding of the Smad3 protein to enhancer I
    Lili Xu
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Immunity 33:313-25. 2010
    ..Thus, control of accessibility and binding of pSmad3 provides a common framework for positive and negative regulation of TGF-β-induced Foxp3 transcription...
  83. ncbi Obtaining human peripheral blood cells
    W Strober
    National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA
    Curr Protoc Immunol . 2001
    ..Cells collected by these procedures can be further separated by techniques described in Chapter 7...
  84. ncbi Trypan blue exclusion test of cell viability
    W Strober
    National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA
    Curr Protoc Immunol . 2001
    ..In the protocol presented here, a viable cell will have a clear cytoplasm whereas a nonviable cell will have a blue cytoplasm...
  85. ncbi Infections in patients with immunodeficiency with thymoma (Good syndrome). Report of 5 cases and review of the literature
    P E Tarr
    National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA
    Medicine (Baltimore) 80:123-33. 2001
    ..GS should be ruled out in patients with thymoma or CVID who develop severe, especially opportunistic, infections. Treatment with intravenous immune globulin is recommended for all patients with GS...
  86. ncbi Wright-Giemsa and nonspecific esterase staining of cells
    W Strober
    National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA
    Curr Protoc Immunol . 2001
    ..Thus, this staining reaction can be used to identify monocytes/macrophages in cell preparations...
  87. ncbi TGF-beta-mediated suppression by CD4+CD25+ T cells is facilitated by CTLA-4 signaling
    Takatoku Oida
    Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA
    J Immunol 177:2331-9. 2006
    ..This suggests that CTLA-4 signaling facilitates TGF-beta-mediated suppression by intensifying the TGF-beta signal at the point of suppressor cell-target cell interaction...
  88. ncbi NOD1 contributes to mouse host defense against Helicobacter pylori via induction of type I IFN and activation of the ISGF3 signaling pathway
    Tomohiro Watanabe
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland 20892, USA
    J Clin Invest 120:1645-62. 2010
    ..pylori and possibly other mucosal infections...
  89. ncbi New insights into the nature of autoinflammatory diseases from mice with Nlrp3 mutations
    Guangxun Meng
    Mucosal Immunity Section, Laboratory of Host Defense, NIAID, NIH Bethesda, MD 20892, USA
    Eur J Immunol 40:649-53. 2010
    ..In this Viewpoint, we will discuss the mechanisms of NLRP3 inflammasome activation and its induction of Th17-cell-dominant immunologic responses...
  90. ncbi Notch1 signaling and regulatory T cell function
    Naoki Asano
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 180:2796-804. 2008
    ..These results are consistent with the conclusion that Notch1 signaling facilitates TGF-beta-mediated effector function of Tregs...
  91. ncbi The signaling function of the IL-13Ralpha2 receptor in the development of gastrointestinal fibrosis and cancer surveillance
    Warren Strober
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Curr Mol Med 9:740-50. 2009
    ....
  92. ncbi Mucosal HIV vaccines: where are we now?
    Liljana Stevceva
    Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA
    Curr HIV Res 2:1-10. 2004
    ..Generations of new vaccines, such as DNA-based vaccines, multipeptide, lipopeptide and alphavirus replicon particles-based vaccines have been created and studied for their efficiency...
  93. ncbi Restoration of tumor immunosurveillance via targeting of interleukin-13 receptor-alpha 2
    Stefan Fichtner-Feigl
    Department of Surgery, University of Regensburg, Regensburg, Germany
    Cancer Res 68:3467-75. 2008
    ..Corroborative data were obtained using the 15-12RM fibrosarcoma model. These studies point to the prevention of metastatic cancer with an available agent with already known clinically acceptable adverse effects and toxicity...
  94. ncbi CD1d-restricted T cell pathways at the epithelial-lymphocyte-luminal interface
    Arthur Kaser
    Division of Gastroenterology, Brigham and Women's Hospital, Boston, MA 02115, USA
    J Pediatr Gastroenterol Nutr 39:S719-22. 2004
    ..In this review, we focus on recent observations in the characteristics of CD1d-restricted pathways in mucosal compartments after a brief introduction to the biology of CD1d and CD1d-restricted T cells...
  95. ncbi Epithelial cells pay a Toll for protection
    Warren Strober
    Nat Med 10:898-900. 2004
  96. ncbi A major quantitative trait locus on mouse chromosome 3 is involved in disease susceptibility in different colitis models
    Michelle E A Borm
    Department of Immunogenetics, Vrije Universiteit Medical Center, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands
    Gastroenterology 128:74-85. 2005
    ..Disease expression differs markedly between inbred strains of mice, indicating genetic control of disease susceptibility. We performed a genome-wide screen to localize the chromosomal regions regulating disease expression...
  97. ncbi Regulatory cells induced by feeding TNP-haptenated colonic protein cross-protect mice from colitis induced by an unrelated hapten
    Monica Boirivant
    Department of Infectious, Parasitic and Immune Mediated Diseases Istituto Superiore di Sanità, Roma, Italy
    Inflamm Bowel Dis 11:48-55. 2005
    ....
  98. ncbi Natural killer T cells in mucosal homeostasis
    Arthur Kaser
    Division of Gastroenterology, Brigham and Women's Hospital, Harvard Medical School, 75 Francis St, Boston, MA 02115, USA
    Ann N Y Acad Sci 1029:154-68. 2004
    ..In this review, we focus on recent observations on the characteristics of CD1d-restricted pathways in mucosal compartments, after a brief introduction into the biology of CD1d and CD1d-restricted T cells...
  99. ncbi Probiotics ameliorate recurrent Th1-mediated murine colitis by inducing IL-10 and IL-10-dependent TGF-beta-bearing regulatory cells
    Claudia Di Giacinto
    Immune-Mediated Diseases Section, Department of Infectious, Parasitic, and Immune-Mediated Diseases, Istituto Superiore di Sanit, Rome, Italy
    J Immunol 174:3237-46. 2005
    ..These studies show that probiotic (VSL#3) administration during a remission period ameliorates the severity of recurrent colitis by inducing an immunoregulatory response involving TGF-beta-bearing regulatory cells...
  100. ncbi Interleukin-13 is the key effector Th2 cytokine in ulcerative colitis that affects epithelial tight junctions, apoptosis, and cell restitution
    Frank Heller
    Department of Gastroenterology, Charit, Campus Benjamin Franklin, Berlin, Germany
    Gastroenterology 129:550-64. 2005
    ..CONCLUSIONS: IL-13 was identified as an important effector cytokine in UC that impairs epithelial barrier function by affecting epithelial apoptosis, tight junctions, and restitution velocity...
  101. ncbi The mechanism of action of probiotics
    Monica Boirivant
    Department of Infectious, Parasitic and Immune Mediated Diseases, Italian National Institute of Health, Rome, Italy
    Curr Opin Gastroenterol 23:679-92. 2007
    ....