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Genomes and GenesSpecies | D V SerrezeSummaryAffiliation: The Jackson Laboratory Country: USA Publications
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Acceleration of type 1 diabetes by a coxsackievirus infection requires a preexisting critical mass of autoreactive T-cells in pancreatic isletsD 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...- 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 miceDavid 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... - Of mice and men: use of animal models to identify possible interventions for the prevention of autoimmune type 1 diabetes in humansDavid 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... - Paralytic autoimmune myositis develops in nonobese diabetic mice made Th1 cytokine-deficient by expression of an IFN-gamma receptor beta-chain transgeneDavid 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... - The role of B lymphocytes as key antigen-presenting cells in the development of T cell-mediated autoimmune type 1 diabetesDavid V Serreze
Jackson Laboratory, Bar Harbor, ME, USA
Curr Dir Autoimmun 6:212-27. 2003 - Autoreactive diabetogenic T-cells in NOD mice can efficiently expand from a greatly reduced precursor poolD 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... - Th1 to Th2 cytokine shifts in nonobese diabetic mice: sometimes an outcome, rather than the cause, of diabetes resistance elicited by immunostimulationD V Serreze
The Jackson Laboratory, Bar Harbor, ME 04609 Department of Medicine, University of Alberta, Edmonton, Canada
J Immunol 166:1352-9. 2001.... - Interferon-gamma receptor signaling is dispensable in the development of autoimmune type 1 diabetes in NOD miceD V Serreze
Jackson Laboratory, Bar Harbor, Maine 04609, USA
Diabetes 49:2007-11. 2000.... 
Unusual resistance of ALR/Lt mouse beta cells to autoimmune destruction: role for beta cell-expressed resistance determinantsC 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...- Identification of a CD8 T cell that can independently mediate autoimmune diabetes development in the complete absence of CD4 T cell helper functionsR T Graser
The Jackson Laboratory, Bar Harbor, ME 04609, USA
J Immunol 164:3913-8. 2000.... - 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 subtypesE 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... - MHC class I-mediated antigen presentation and induction of CD8+ cytotoxic T-cell responses in autoimmune diabetes-prone NOD miceD 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... - Reevaluation of the major histocompatibility complex genes of the NOD-progenitor CTS/Shi strainC 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... - Initiation of autoimmune diabetes in NOD/Lt mice is MHC class I-dependentD V Serreze
The Jackson Laboratory, Bar Harbor, ME 04609, USA
J Immunol 158:3978-86. 1997.... - Subcongenic analysis of the Idd13 locus in NOD/Lt mice: evidence for several susceptibility genes including a possible diabetogenic role for beta 2-microglobulinD 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... - Hematopoietic stem-cell defects underlying abnormal macrophage development and maturation in NOD/Lt mice: defective regulation of cytokine receptors and protein kinase CD 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... - Mapping to chromosomes 1 and 12 of mouse homologs of human protein tyrosine phosphatase, receptor-type, related genes encoding pancreatic beta cell autoantigensE H Leiter
Jackson Laboratory, Bar Harbor, Maine 04609-1500, USA
Mamm Genome 8:949-50. 1997 - Unexpected functional consequences of xenogeneic transgene expression in beta-cells of NOD miceE 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... - Emv30null NOD-scid mice. An improved host for adoptive transfer of autoimmune diabetes and growth of human lymphohematopoietic cellsD 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).. - 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 epitheliumD 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).. - Major histocompatibility complex class I-deficient NOD-B2mnull mice are diabetes and insulitis resistantD 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... - Conditioning the genome identifies additional diabetes resistance loci in Type I diabetes resistant NOR/Lt miceP 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... - Beta cell expression of endogenous xenotropic retrovirus distinguishes diabetes-susceptible NOD/Lt from resistant NON/Lt miceH 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... - Molecular mimicry between insulin and retroviral antigen p73. Development of cross-reactive autoantibodies in sera of NOD and C57BL/KsJ db/db miceD 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).. - 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 dietJ 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... - MHC characterization of ALR and ALS mice: respective similarities to the NOD and NON strainsR T Graser
The Jackson Laboratory, 600 Main St, Bar Harbor, ME 04609, USA
Immunogenetics 49:722-6. 1999 - Use of recombinant congenic and congenic strains of NOD mice to identify a new insulin-dependent diabetes resistance geneD 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... - Defects in limb, craniofacial, and thymic development in Jagged2 mutant miceR 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... - Genetic control of murine invariant natural killer T-cell development dynamically differs dependent on the examined tissue typeY 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... - Genetic control of diabetogenesis in NOD/Lt mice. Development and analysis of congenic stocksM Prochazka
Jackson Laboratory, Bar Harbor, ME 04609
Diabetes 38:1446-55. 1989..abstract truncated at 400 words).. - 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) complexDarcy 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... - CD38 is required for the peripheral survival of immunotolerogenic CD4+ invariant NK T cells in nonobese diabetic miceYi 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... - Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashionJing 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... - Invasion of the killer B's in type 1 diabetesPablo 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... - Novel leptin receptor mutation in NOD/LtJ mice suppresses type 1 diabetes progression: II. Immunologic analysisChul Ho Lee
The Jackson Laboratory, 600 Main St, Bar Harbor, ME 04609, USA
Diabetes 55:171-8. 2006.... - The good turned ugly: immunopathogenic basis for diabetogenic CD8+ T cells in NOD miceTeresa 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... - 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 rolesBao-You Xu
Department of Pathology, IWK Health Centre, Halifax, Nova Scotia, Canada
Transplantation 80:402-9. 2005..Graft rejection requires CD4 T-cells, is facilitated by B-cells, and does not require CD8 T-cells... - Partial versus full allogeneic hemopoietic chimerization is a preferential means to inhibit type 1 diabetes as the latter induces generalized immunosuppressionDavid V Serreze
The Jackson Laboratory, Bar Harbor, ME 04609, USA
J Immunol 177:6675-84. 2006.... - Genes within the Idd5 and Idd9/11 diabetes susceptibility loci affect the pathogenic activity of B cells in nonobese diabetic micePablo 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... - Rapid identification of MHC class I-restricted antigens relevant to autoimmune diabetes using retrogenic T cellsRodolfo 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... - Selective delivery of beta cell antigen to dendritic cells in vivo leads to deletion and tolerance of autoreactive CD8+ T cells in NOD miceArunika 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... - 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 miceDavid 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... - In vivo cytotoxicity of insulin-specific CD8+ T-cells in HLA-A*0201 transgenic NOD miceIrene 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... - Subcongenic analysis of genetic basis for impaired development of invariant NKT cells in NOD miceYi 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... - "Humanized" HLA transgenic NOD mice to identify pancreatic beta cell autoantigens of potential clinical relevance to type 1 diabetesDavid 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... - Interleukin-2 gene variation impairs regulatory T cell function and causes autoimmunityJun 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... - Cellular expression requirements for inhibition of type 1 diabetes by a dominantly protective major histocompatibility complex haplotypeYi 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... - HLA-A*0201-restricted T cells from humanized NOD mice recognize autoantigens of potential clinical relevance to type 1 diabetesToshiyuki 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... - Activated NKT cells inhibit autoimmune diabetes through tolerogenic recruitment of dendritic cells to pancreatic lymph nodesYi-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... - Genetic analysis of resistance to Type-1 Diabetes in ALR/Lt mice, a NOD-related strain with defenses against autoimmune-mediated diabetogenic stressClayton 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... - Genetic separation of the transplantation tolerance and autoimmune phenotypes in NOD miceTodd 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 - Tracking autoimmune T cells in diabetesDavid 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... - Genetic disassociation of autoimmunity and resistance to costimulation blockade-induced transplantation tolerance in nonobese diabetic miceTodd 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... - Identification of the beta cell antigen targeted by a prevalent population of pathogenic CD8+ T cells in autoimmune diabetesScott 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... - Adenovirus early region 3 antiapoptotic 10.4K, 14.5K, and 14.7K genes decrease the incidence of autoimmune diabetes in NOD miceMelissa 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... - NOD congenic mice genetically protected from autoimmune diabetes remain resistant to transplantation tolerance inductionTodd Pearson
Program in Immunology and Virology, University of Massachusetts Medical School, Worcester 01605, USA
Diabetes 52:321-6. 2003.... - The preferential ability of B lymphocytes to act as diabetogenic APC in NOD mice depends on expression of self-antigen-specific immunoglobulin receptorsPablo 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... - During the early prediabetic period in NOD mice, the pathogenic CD8(+) T-cell population comprises multiple antigenic specificitiesTeresa 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... - Adenovirus early region 3 transgenes expressed in beta cells prevent autoimmune diabetes in nonobese diabetic mice: effects of deleting the adenovirus death protein 11.6KMelissa 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... - B cell selection defects underlie the development of diabetogenic APCs in nonobese diabetic micePablo 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... - Autoimmune diabetes and resistance to xenograft transplantation tolerance in NOD miceEthel 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... - Diabetes acceleration or prevention by a coxsackievirus B4 infection: critical requirements for both interleukin-4 and gamma interferonDavid 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... - Functional evidence for the mediation of diabetogenic T cell responses by HLA-A2.1 MHC class I molecules through transgenic expression in NOD miceMichele 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... - Individual nonobese diabetic mice exhibit unique patterns of CD8+ T cell reactivity to three islet antigens, including the newly identified widely expressed dystrophia myotonica kinaseScott 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... - CTLA-4-Ig activates forkhead transcription factors and protects dendritic cells from oxidative stress in nonobese diabetic miceFrancesca Fallarino
Department of Experimental Medicine, University of Perugia, Perugia 06126, Italy
J Exp Med 200:1051-62. 2004.... - Enhanced pathogenicity of diabetogenic T cells escaping a non-MHC gene-controlled near death experienceCaroline Morgane Choisy-Rossi
The Jackson Laboratory, Bar Harbor, ME 04609, USA
J Immunol 173:3791-800. 2004.... - Requirement for both H-2Db and H-2Kd for the induction of diabetes by the promiscuous CD8+ T cell clonotype AI4Toshiyuki 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... - Islet allograft survival induced by costimulation blockade in NOD mice is controlled by allelic variants of Idd3Todd Pearson
The University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
Diabetes 53:1972-8. 2004.... - 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... - 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 - By altering ocular immune privilege, bone marrow-derived cells pathogenically contribute to DBA/2J pigmentary glaucomaJun-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...