D V Serreze

Summary

Affiliation: The Jackson Laboratory
Country: USA

Publications

  1. ncbi request reprint Acceleration of type 1 diabetes by a coxsackievirus infection requires a preexisting critical mass of autoreactive T-cells in pancreatic islets
    D V Serreze
    Jackson Laboratory, Bar Harbor, Maine 04609, USA
    Diabetes 49:708-11. 2000
  2. ncbi request reprint MHC class II molecules play a role in the selection of autoreactive class I-restricted CD8 T cells that are essential contributors to type 1 diabetes development in nonobese diabetic mice
    David V Serreze
    The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA
    J Immunol 172:871-9. 2004
  3. ncbi request reprint Of mice and men: use of animal models to identify possible interventions for the prevention of autoimmune type 1 diabetes in humans
    David V Serreze
    The Jackson Laboratory, 600 Main St, Bar Harbor, ME 04609, USA
    Trends Immunol 26:603-7. 2005
  4. ncbi request reprint Paralytic autoimmune myositis develops in nonobese diabetic mice made Th1 cytokine-deficient by expression of an IFN-gamma receptor beta-chain transgene
    David V Serreze
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    J Immunol 170:2742-9. 2003
  5. ncbi request reprint The role of B lymphocytes as key antigen-presenting cells in the development of T cell-mediated autoimmune type 1 diabetes
    David V Serreze
    Jackson Laboratory, Bar Harbor, ME, USA
    Curr Dir Autoimmun 6:212-27. 2003
  6. ncbi request reprint Autoreactive diabetogenic T-cells in NOD mice can efficiently expand from a greatly reduced precursor pool
    D V Serreze
    The Jackson Laboratory, Bar Harbor, Maine 04609, USA
    Diabetes 50:1992-2000. 2001
  7. ncbi request reprint Th1 to Th2 cytokine shifts in nonobese diabetic mice: sometimes an outcome, rather than the cause, of diabetes resistance elicited by immunostimulation
    D V Serreze
    The Jackson Laboratory, Bar Harbor, ME 04609 Department of Medicine, University of Alberta, Edmonton, Canada
    J Immunol 166:1352-9. 2001
  8. ncbi request reprint Interferon-gamma receptor signaling is dispensable in the development of autoimmune type 1 diabetes in NOD mice
    D V Serreze
    Jackson Laboratory, Bar Harbor, Maine 04609, USA
    Diabetes 49:2007-11. 2000
  9. pmc Unusual resistance of ALR/Lt mouse beta cells to autoimmune destruction: role for beta cell-expressed resistance determinants
    C E Mathews
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    Proc Natl Acad Sci U S A 98:235-40. 2001
  10. ncbi request reprint Identification of a CD8 T cell that can independently mediate autoimmune diabetes development in the complete absence of CD4 T cell helper functions
    R T Graser
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    J Immunol 164:3913-8. 2000

Collaborators

Detail Information

Publications71

  1. ncbi request reprint Acceleration of type 1 diabetes by a coxsackievirus infection requires a preexisting critical mass of autoreactive T-cells in pancreatic islets
    D V Serreze
    Jackson Laboratory, Bar Harbor, Maine 04609, USA
    Diabetes 49:708-11. 2000
    ..These findings indicate that the timing of a coxsackievirus infection, rather than its simple presence or absence, may have important etiological implications for the development of T-cell-mediated autoimmune type 1 diabetes in humans...
  2. ncbi request reprint MHC class II molecules play a role in the selection of autoreactive class I-restricted CD8 T cells that are essential contributors to type 1 diabetes development in nonobese diabetic mice
    David V Serreze
    The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA
    J Immunol 172:871-9. 2004
    ..These findings provide insights to how particular MHC class I and class II variants interactively regulate the development of diabetogenic T cells and the TCR promiscuity of such autoreactive effectors...
  3. ncbi request reprint Of mice and men: use of animal models to identify possible interventions for the prevention of autoimmune type 1 diabetes in humans
    David V Serreze
    The Jackson Laboratory, 600 Main St, Bar Harbor, ME 04609, USA
    Trends Immunol 26:603-7. 2005
    ..Based on this information, the possible positive and negative aspects of various antigen-specific and non-specific immunotherapies, which could potentially prevent the onset of T1D in at risk individuals, are discussed...
  4. ncbi request reprint Paralytic autoimmune myositis develops in nonobese diabetic mice made Th1 cytokine-deficient by expression of an IFN-gamma receptor beta-chain transgene
    David V Serreze
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    J Immunol 170:2742-9. 2003
    ..This should raise a cautionary note when considering the use of protocols that induce alterations in cytokine balances as a means of blocking progression to overt T1D in at-risk humans...
  5. ncbi request reprint The role of B lymphocytes as key antigen-presenting cells in the development of T cell-mediated autoimmune type 1 diabetes
    David V Serreze
    Jackson Laboratory, Bar Harbor, ME, USA
    Curr Dir Autoimmun 6:212-27. 2003
  6. ncbi request reprint Autoreactive diabetogenic T-cells in NOD mice can efficiently expand from a greatly reduced precursor pool
    D V Serreze
    The Jackson Laboratory, Bar Harbor, Maine 04609, USA
    Diabetes 50:1992-2000. 2001
    ..This might allow diabetogenic T-cells in NOD mice to undergo an efficient expansion before encountering antigen, which would represent an important and previously unconsidered aspect of pathogenesis...
  7. ncbi request reprint Th1 to Th2 cytokine shifts in nonobese diabetic mice: sometimes an outcome, rather than the cause, of diabetes resistance elicited by immunostimulation
    D V Serreze
    The Jackson Laboratory, Bar Harbor, ME 04609 Department of Medicine, University of Alberta, Edmonton, Canada
    J Immunol 166:1352-9. 2001
    ....
  8. ncbi request reprint Interferon-gamma receptor signaling is dispensable in the development of autoimmune type 1 diabetes in NOD mice
    D V Serreze
    Jackson Laboratory, Bar Harbor, Maine 04609, USA
    Diabetes 49:2007-11. 2000
    ....
  9. pmc Unusual resistance of ALR/Lt mouse beta cells to autoimmune destruction: role for beta cell-expressed resistance determinants
    C E Mathews
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    Proc Natl Acad Sci U S A 98:235-40. 2001
    ..In conclusion, the ALR mouse presents a unique opportunity to identify dominant IDDM resistance determinants expressed at the beta cell level...
  10. ncbi request reprint Identification of a CD8 T cell that can independently mediate autoimmune diabetes development in the complete absence of CD4 T cell helper functions
    R T Graser
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    J Immunol 164:3913-8. 2000
    ....
  11. ncbi request reprint Inhibition of autoimmune diabetes in nonobese diabetic mice by transgenic restoration of H2-E MHC class II expression: additive, but unequal, involvement of multiple APC subtypes
    E A Johnson
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    J Immunol 167:2404-10. 2001
    ..This raises a high threshold for success in future intervention protocols designed to inhibit IDDM by introduction of putatively protective MHC molecules into hemopoietic precursors of APC...
  12. ncbi request reprint MHC class I-mediated antigen presentation and induction of CD8+ cytotoxic T-cell responses in autoimmune diabetes-prone NOD mice
    D V Serreze
    Jackson Laboratory, Bar Harbor, Maine 04609, USA
    Diabetes 45:902-8. 1996
    ..The absence of female-specific Tap gene defects also indicates this cannot account for the reduced male incidence of IDDM in some NOD mouse colonies...
  13. ncbi request reprint Reevaluation of the major histocompatibility complex genes of the NOD-progenitor CTS/Shi strain
    C E Mathews
    The Jackson Laboratory, Bar Harbor, Maine 04609, USA
    Diabetes 49:131-4. 2000
    ..These results in mouse model systems show that multiple MHC genes confer diabetes resistance and suggest that at least one of the protective MHC or MHC-linked genes in CTS mice may be at the H2-D end of the complex...
  14. ncbi request reprint Initiation of autoimmune diabetes in NOD/Lt mice is MHC class I-dependent
    D V Serreze
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    J Immunol 158:3978-86. 1997
    ....
  15. ncbi request reprint Subcongenic analysis of the Idd13 locus in NOD/Lt mice: evidence for several susceptibility genes including a possible diabetogenic role for beta 2-microglobulin
    D V Serreze
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    J Immunol 160:1472-8. 1998
    ..Since trans-interactions between relatively common and functionally normal allelic variants may contribute to IDDM in NOD mice, the search for Idd genes in humans should not be limited to functionally defective variants...
  16. pmc Hematopoietic stem-cell defects underlying abnormal macrophage development and maturation in NOD/Lt mice: defective regulation of cytokine receptors and protein kinase C
    D V Serreze
    Jackson Laboratory, Bar Harbor, ME 04609
    Proc Natl Acad Sci U S A 90:9625-9. 1993
    ..Thus, failure to develop functionally mature monocytes may be of pathogenic significance in NOD mice...
  17. ncbi request reprint Mapping to chromosomes 1 and 12 of mouse homologs of human protein tyrosine phosphatase, receptor-type, related genes encoding pancreatic beta cell autoantigens
    E H Leiter
    Jackson Laboratory, Bar Harbor, Maine 04609 1500, USA
    Mamm Genome 8:949-50. 1997
  18. ncbi request reprint Unexpected functional consequences of xenogeneic transgene expression in beta-cells of NOD mice
    E H Leiter
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    Diabetes Obes Metab 9:14-22. 2007
    ..These findings emphasize the need for careful characterization of genetically manipulated NOD mouse stocks to insure that model characteristics have not been compromised...
  19. ncbi request reprint Emv30null NOD-scid mice. An improved host for adoptive transfer of autoimmune diabetes and growth of human lymphohematopoietic cells
    D V Serreze
    Jackson Laboratory, Bar Harbor, Maine 04609, USA
    Diabetes 44:1392-8. 1995
    ..Significantly, the ability of standard NOD T-cells to transfer IDDM to the Emv30null NOD-scid stock was not impaired.(ABSTRACT TRUNCATED AT 250 WORDS)..
  20. ncbi request reprint Development of diabetogenic T cells from NOD/Lt marrow is blocked when an allo-H-2 haplotype is expressed on cells of hemopoietic origin, but not on thymic epithelium
    D V Serreze
    Jackson Laboratory, Bar Harbor, ME 04609
    J Immunol 147:1222-9. 1991
    ..Skin grafting confirmed that all reconstitution classes of MHC heterozygous recipients were tolerant to the H-2nb1 haplotype.(ABSTRACT TRUNCATED AT 400 WORDS)..
  21. ncbi request reprint Major histocompatibility complex class I-deficient NOD-B2mnull mice are diabetes and insulitis resistant
    D V Serreze
    Jackson Laboratory, Bar Harbor, ME 04609
    Diabetes 43:505-9. 1994
    ..Thus, elimination of cell surface MHC class I expression with a disrupted B2m gene blocks autoimmune diabetes in NOD/Lt mice, without engendering a separate, distinct form of glucose intolerance...
  22. ncbi request reprint Conditioning the genome identifies additional diabetes resistance loci in Type I diabetes resistant NOR/Lt mice
    P C Reifsnyder
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    Genes Immun 6:528-38. 2005
    ..11. These findings emphasize the value for diabetes gene discovery of stratifying not only MHC loci conferring the highest relative risk but also as many as possible of the non-MHC loci presumed to contribute significantly...
  23. pmc Beta cell expression of endogenous xenotropic retrovirus distinguishes diabetes-susceptible NOD/Lt from resistant NON/Lt mice
    H R Gaskins
    Jackson Laboratory, Bar Harbor, Maine 04609
    J Clin Invest 90:2220-7. 1992
    ..The potential pathogenic role of retroviral gene expression in NOD beta cells is discussed...
  24. ncbi request reprint Molecular mimicry between insulin and retroviral antigen p73. Development of cross-reactive autoantibodies in sera of NOD and C57BL/KsJ db/db mice
    D V Serreze
    Jackson Laboratory, Bar Harbor, ME 04609
    Diabetes 37:351-8. 1988
    ..Absorption studies indicated that autoantibodies against p73 recognized a common epitope on insulin and IgE-binding factor. The potential significance of this molecular mimicry is discussed.(ABSTRACT TRUNCATED AT 250 WORDS)..
  25. pmc Comparative therapeutic effects of orally administered 1,25-dihydroxyvitamin D(3) and 1alpha-hydroxyvitamin D(3) on type-1 diabetes in non-obese diabetic mice fed a normal-calcaemic diet
    J P Driver
    The Jackson Laboratory, Bar Harbor, ME, USA
    Clin Exp Immunol 151:76-85. 2008
    ..In future, the dietary supplementation of novel low-calcaemic D3 analogues may enable their continuous delivery at levels that inhibit T1D development in susceptible humans consuming normal levels of Ca...
  26. ncbi request reprint MHC characterization of ALR and ALS mice: respective similarities to the NOD and NON strains
    R T Graser
    The Jackson Laboratory, 600 Main St, Bar Harbor, ME 04609, USA
    Immunogenetics 49:722-6. 1999
  27. pmc Use of recombinant congenic and congenic strains of NOD mice to identify a new insulin-dependent diabetes resistance gene
    D V Serreze
    Jackson Laboratory, Bar Harbor, Maine 04609
    J Exp Med 180:1553-8. 1994
    ..Our analysis shows the utility of RCS and congenic stocks for the identification and isolation of non-MHC genes with strong antidiabetogenic functions...
  28. pmc Defects in limb, craniofacial, and thymic development in Jagged2 mutant mice
    R Jiang
    The Jackson Laboratory, Bar Harbor, Maine 04609 USA
    Genes Dev 12:1046-57. 1998
    ..These results demonstrate that Notch signaling mediated by Jag2 plays an essential role during limb, craniofacial, and thymic development in mice...
  29. pmc Genetic control of murine invariant natural killer T-cell development dynamically differs dependent on the examined tissue type
    Y G Chen
    The Jackson Laboratory, Bar Harbor, ME, USA
    Genes Immun 13:164-74. 2012
    ..Genome-wide association studies across strains identified only partially overlapping loci associated with variability of iNKT cell frequencies within and between differing anatomical sites...
  30. ncbi request reprint Genetic control of diabetogenesis in NOD/Lt mice. Development and analysis of congenic stocks
    M Prochazka
    Jackson Laboratory, Bar Harbor, ME 04609
    Diabetes 38:1446-55. 1989
    ..abstract truncated at 400 words)..
  31. ncbi request reprint Major histocompatibility complex-linked diabetes susceptibility in NOD/Lt mice: subcongenic analysis localizes a component of Idd16 at the H2-D end of the diabetogenic H2(g7) complex
    Darcy P Pomerleau
    The Jackson Laboratory, 600 Main St, Bar Harbor, ME 04609, USA
    Diabetes 54:1603-6. 2005
    ..33 mB, distinguishing D.R2 from D.R3. Evidence supporting the candidacy of the ALR/CTS-shared H2-D(dx) MHC class I variant present in both diabetes-resistant stocks, but not the susceptible stock, is discussed...
  32. ncbi request reprint CD38 is required for the peripheral survival of immunotolerogenic CD4+ invariant NK T cells in nonobese diabetic mice
    Yi Guang Chen
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    J Immunol 177:2939-47. 2006
    ..Therefore, this study documents a previously unrecognized role for CD38 in maintaining survival of an iNKT cell subset that preferentially contributes to the maintenance of immunological tolerance...
  33. ncbi request reprint Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashion
    Jing Chen
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    J Immunol 176:4590-9. 2006
    ..Unexpectedly, diabetes development in the combined CD38/ART2 stock was strongly suppressed, possibly through epistatic interactions between genes linked to the targeted CD38 on Chromosome 5 and the ART2 complex on Chromosome 7...
  34. ncbi request reprint Invasion of the killer B's in type 1 diabetes
    Pablo A Silveira
    Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst NSW 2010, Australia
    Front Biosci 12:2183-93. 2007
    ..This review will focus on the under appreciated role B cells play in T1D development not only in NOD mice, but also potentially in humans...
  35. ncbi request reprint Novel leptin receptor mutation in NOD/LtJ mice suppresses type 1 diabetes progression: II. Immunologic analysis
    Chul Ho Lee
    The Jackson Laboratory, 600 Main St, Bar Harbor, ME 04609, USA
    Diabetes 55:171-8. 2006
    ....
  36. ncbi request reprint The good turned ugly: immunopathogenic basis for diabetogenic CD8+ T cells in NOD mice
    Teresa P DiLorenzo
    Department of Microbiology, Division of Endocrinology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Immunol Rev 204:250-63. 2005
    ..As CD8(+) T cells are suspected contributors to beta-cell demise in humans, continued exploration of these critical areas could very possibly lead to tangible benefits for T1D patients and at-risk individuals...
  37. ncbi request reprint Rapid destruction of encapsulated islet xenografts by NOD mice is CD4-dependent and facilitated by B-cells: innate immunity and autoimmunity do not play significant roles
    Bao You Xu
    Department of Pathology, IWK Health Centre, Halifax, Nova Scotia, Canada
    Transplantation 80:402-9. 2005
    ..Spontaneously diabetic NOD mice rapidly reject microencapsulated islet xenografts via an intense pericapsular inflammatory response...
  38. ncbi request reprint Partial versus full allogeneic hemopoietic chimerization is a preferential means to inhibit type 1 diabetes as the latter induces generalized immunosuppression
    David V Serreze
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    J Immunol 177:6675-84. 2006
    ....
  39. pmc Genes within the Idd5 and Idd9/11 diabetes susceptibility loci affect the pathogenic activity of B cells in nonobese diabetic mice
    Pablo A Silveira
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    J Immunol 177:7033-41. 2006
    ..Interestingly, both Idd5.1/5.2 and Idd9/11-resistance loci were found to normalize this B cell tolerogenic process, which may represent a mechanism contributing to the inhibition of T1D...
  40. pmc Rapid identification of MHC class I-restricted antigens relevant to autoimmune diabetes using retrogenic T cells
    Rodolfo José Chaparro
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    J Immunol Methods 335:106-15. 2008
    ..Our method is the first to combine the speed of Rg technology with an optimized in vitro Rg T cell expansion protocol to enable the rapid discovery of T cell antigens...
  41. pmc Selective delivery of beta cell antigen to dendritic cells in vivo leads to deletion and tolerance of autoreactive CD8+ T cells in NOD mice
    Arunika Mukhopadhaya
    Departments of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 105:6374-9. 2008
    ..Our results provide support for the development of DC targeting of self antigens for treatment of chronic T cell-mediated autoimmune diseases...
  42. ncbi request reprint Through regulation of TCR expression levels, an Idd7 region gene(s) interactively contributes to the impaired thymic deletion of autoreactive diabetogenic CD8+ T cells in nonobese diabetic mice
    David V Serreze
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    J Immunol 180:3250-9. 2008
    ..These findings provide further insight to how susceptibility genes, both within and outside the MHC, may interact to elicit autoreactive T cell responses mediating T1D development in both NOD mice and human patients...
  43. ncbi request reprint In vivo cytotoxicity of insulin-specific CD8+ T-cells in HLA-A*0201 transgenic NOD mice
    Irene Jarchum
    Albert Einstein College of Medicine, Department of Microbiology and Immunology, 1300 Morris Park Ave, Bronx, NY 10461, USA
    Diabetes 56:2551-60. 2007
    ..The development of peptide-based therapeutic reagents that target islet-reactive CD8(+) T-cells will require the identification of disease-relevant epitopes...
  44. ncbi request reprint Subcongenic analysis of genetic basis for impaired development of invariant NKT cells in NOD mice
    Yi Guang Chen
    The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA
    Immunogenetics 59:705-12. 2007
    ..Subcongenic analyses indicated that at least two genes within the Idd13 region regulate iNKT cell numbers. These results further define the genetic basis for numerical iNKT cell defects contributing to T1D development in NOD mice...
  45. ncbi request reprint "Humanized" HLA transgenic NOD mice to identify pancreatic beta cell autoantigens of potential clinical relevance to type 1 diabetes
    David V Serreze
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    Ann N Y Acad Sci 1103:103-11. 2007
    ..1-restricted IGRP peptides can be used in a tolerance-inducing protocol that inhibits T1D development in NOD. beta2m-.HHD mice. If so, this knowledge could ultimately lead to the development of a similar T1D prevention protocol in humans...
  46. pmc Interleukin-2 gene variation impairs regulatory T cell function and causes autoimmunity
    Jun Yamanouchi
    Julia McFarlane Diabetes Research Centre JMDRC and Department of Microbiology and Infectious Diseases, Institute of Inflammation, Infection and Immunity, Faculty of Medicine, The University of Calgary, Calgary, Alberta T2N 4N1, Canada
    Nat Genet 39:329-37. 2007
    ..Reduced IL-2 production achieved by either genetic mechanism correlates with reduced function of CD4(+) CD25(+) regulatory T cells, which are critical for maintaining immune homeostasis...
  47. ncbi request reprint Cellular expression requirements for inhibition of type 1 diabetes by a dominantly protective major histocompatibility complex haplotype
    Yi Guang Chen
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    Diabetes 56:424-30. 2007
    ..At this engraftment level, H2(nb1)-expressing dendritic cells and macrophages mediated virtually complete deletion of a highly pathogenic CD8 T-cell population...
  48. ncbi request reprint HLA-A*0201-restricted T cells from humanized NOD mice recognize autoantigens of potential clinical relevance to type 1 diabetes
    Toshiyuki Takaki
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    J Immunol 176:3257-65. 2006
    ..In particular, the identified antigenic peptides represent promising tools to explore the potential importance of IGRP in the development of human T1D...
  49. ncbi request reprint Activated NKT cells inhibit autoimmune diabetes through tolerogenic recruitment of dendritic cells to pancreatic lymph nodes
    Yi Guang Chen
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    J Immunol 174:1196-204. 2005
    ..Hence, activated NKT cells elicit diabetes protection in NOD mice by producing a soluble factor(s) that induces DC maturation and accumulation in PLNs, where they subsequently recruit and tolerize pathogenic T cells...
  50. ncbi request reprint Genetic analysis of resistance to Type-1 Diabetes in ALR/Lt mice, a NOD-related strain with defenses against autoimmune-mediated diabetogenic stress
    Clayton E Mathews
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    Immunogenetics 55:491-6. 2003
    ..Two additional ALR-contributed resistance loci may be ALR-specific and contribute to this strain's ability to dissipate free-radical stress...
  51. ncbi request reprint Genetic separation of the transplantation tolerance and autoimmune phenotypes in NOD mice
    Todd Pearson
    Program in Immunology and Virology, at The University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA
    Rev Endocr Metab Disord 4:255-61. 2003
  52. pmc Tracking autoimmune T cells in diabetes
    David V Serreze
    The Jackson Laboratory, 600 Main Street, Bar Harbor, Maine 04609, USA
    J Clin Invest 112:826-8. 2003
    ..Methodologies to track the development, migration, and functional activation of one class of such T cells (CD4 T cells) have been limited. However, it now appears that this limitation has been overcome...
  53. ncbi request reprint Genetic disassociation of autoimmunity and resistance to costimulation blockade-induced transplantation tolerance in nonobese diabetic mice
    Todd Pearson
    Program in Immunology and Virology, University of Massachusetts Medical School, Worcester, MA 01655, USA
    J Immunol 171:185-95. 2003
    ..The outcomes of tolerance induction protocols tested in NOD mice may not accurately predict outcomes in human subjects...
  54. pmc Identification of the beta cell antigen targeted by a prevalent population of pathogenic CD8+ T cells in autoimmune diabetes
    Scott M Lieberman
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 100:8384-8. 2003
    ..The human IGRP gene maps to a diabetes susceptibility locus, suggesting that IGRP also may be an antigen for pathogenic T cells in human type 1 diabetes and, thus, a new, potential target for diagnostic and therapeutic approaches...
  55. ncbi request reprint Adenovirus early region 3 antiapoptotic 10.4K, 14.5K, and 14.7K genes decrease the incidence of autoimmune diabetes in NOD mice
    Melissa A Pierce
    The Jackson Laboratory, 600 Main Street, Bar Harbor, Maine 04609, USA
    Diabetes 52:1119-27. 2003
    ..They also demonstrate that the antiapoptotic E3 genes most effectively protect pancreatic beta-cells from diabetogenic immune responses...
  56. ncbi request reprint NOD congenic mice genetically protected from autoimmune diabetes remain resistant to transplantation tolerance induction
    Todd Pearson
    Program in Immunology and Virology, University of Massachusetts Medical School, Worcester 01605, USA
    Diabetes 52:321-6. 2003
    ....
  57. ncbi request reprint The preferential ability of B lymphocytes to act as diabetogenic APC in NOD mice depends on expression of self-antigen-specific immunoglobulin receptors
    Pablo A Silveira
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    Eur J Immunol 32:3657-66. 2002
    ..Hence, defects in B lymphocyte, as well as T lymphocyte, tolerance induction mechanisms may contribute to T1D in NOD mice...
  58. ncbi request reprint During the early prediabetic period in NOD mice, the pathogenic CD8(+) T-cell population comprises multiple antigenic specificities
    Teresa P DiLorenzo
    Department of Microbiology and Infectious Diseases, Faculty of Medicine, University of Calgary, Calgary, Alberta, T2N 4N1, Canada
    Clin Immunol 105:332-41. 2002
    ..NIT-1 cells represent an unlimited peptide source that will allow for the future isolation and sequencing of the novel multiple epitopes targeted early in the autoimmune response by pathogenic CD8(+) T cells...
  59. pmc Adenovirus early region 3 transgenes expressed in beta cells prevent autoimmune diabetes in nonobese diabetic mice: effects of deleting the adenovirus death protein 11.6K
    Melissa A Pierce
    The Jackson Laboratory, Bar Harbor, Maine 04609, USA
    J Virol 79:619-21. 2005
    ..Significantly, deletion of ADP did not improve the diabetes-protective effect of an E3 gene cassette...
  60. pmc B cell selection defects underlie the development of diabetogenic APCs in nonobese diabetic mice
    Pablo A Silveira
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    J Immunol 172:5086-94. 2004
    ..The defective induction of B cell tolerance to soluble autoantigens is most likely responsible for the generation of diabetogenic APC in NOD mice...
  61. ncbi request reprint Autoimmune diabetes and resistance to xenograft transplantation tolerance in NOD mice
    Ethel J Gordon
    University of Massachusetts Medical School, Diabetes Division, Department of Medicine, 373 Plantation St, Biotech 2, Suite 218, Worcester, MA 01605, USA
    Diabetes 54:107-15. 2005
    ..We conclude that the resistance of NOD mice to xenograft tolerance induction involves some mechanisms that also participate in the expression of autoimmunity and other mechanisms that are distinct...
  62. pmc Diabetes acceleration or prevention by a coxsackievirus B4 infection: critical requirements for both interleukin-4 and gamma interferon
    David V Serreze
    Department of Pathology, University of Florida, Box 100275 JHMHC, 1600 SW Archer Rd, Gainesville, FL 32610, USA
    J Virol 79:1045-52. 2005
    ..The protective mechanism against diabetes elicited in NOD mice infected with CVB4 prior to the development of a critical threshold level of insulitis requires neither IL-4 nor IFN-gamma...
  63. pmc Functional evidence for the mediation of diabetogenic T cell responses by HLA-A2.1 MHC class I molecules through transgenic expression in NOD mice
    Michele P Marron
    The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA
    Proc Natl Acad Sci U S A 99:13753-8. 2002
    ..These findings provide the first functional evidence that certain human MHC class I molecules can contribute to the development of T1D...
  64. ncbi request reprint Individual nonobese diabetic mice exhibit unique patterns of CD8+ T cell reactivity to three islet antigens, including the newly identified widely expressed dystrophia myotonica kinase
    Scott M Lieberman
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    J Immunol 173:6727-34. 2004
    ..Importantly, the antigenic peptide is naturally processed and presented by DMK-transfected cells. DMK is a widely expressed protein that is nonetheless the target of a beta cell-specific autoimmune response...
  65. pmc CTLA-4-Ig activates forkhead transcription factors and protects dendritic cells from oxidative stress in nonobese diabetic mice
    Francesca Fallarino
    Department of Experimental Medicine, University of Perugia, Perugia 06126, Italy
    J Exp Med 200:1051-62. 2004
    ....
  66. ncbi request reprint Enhanced pathogenicity of diabetogenic T cells escaping a non-MHC gene-controlled near death experience
    Caroline Morgane Choisy-Rossi
    The Jackson Laboratory, Bar Harbor, ME 04609, USA
    J Immunol 173:3791-800. 2004
    ....
  67. ncbi request reprint Requirement for both H-2Db and H-2Kd for the induction of diabetes by the promiscuous CD8+ T cell clonotype AI4
    Toshiyuki Takaki
    Departments of Microbiology and Immunology, and Medicine Division of Endocrinology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    J Immunol 173:2530-41. 2004
    ..Our identification of a ligand for AI4-like T cells will facilitate further characterization and manipulation of this pathogenic and promiscuous T cell population...
  68. ncbi request reprint Islet allograft survival induced by costimulation blockade in NOD mice is controlled by allelic variants of Idd3
    Todd Pearson
    The University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    Diabetes 53:1972-8. 2004
    ....
  69. ncbi request reprint Islet cell autoimmunity and transplantation tolerance: two distinct mechanisms?
    Todd Pearson
    Program in Immunology and Virology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    Ann N Y Acad Sci 1005:148-56. 2003
    ..We believe that the recent discoveries we describe will have important implications for the development of tolerance-based transplantation therapies and their translation from the laboratory to the clinic...
  70. ncbi request reprint Was there type 1 diabetes in the Olduvai Gorge?
    David V Serreze
    The Jackson Laboratory, Bar Harbor, Maine, USA
    Adv Exp Med Biol 552:322-5. 2004
  71. pmc By altering ocular immune privilege, bone marrow-derived cells pathogenically contribute to DBA/2J pigmentary glaucoma
    Jun Song Mo
    The Howard Hughes Medical Institute, The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA
    J Exp Med 197:1335-44. 2003
    ..These results suggest previously unsuspected roles for bone marrow-derived cells and ocular immune privilege in the pathogenesis of PG...