Multiple differences in gene expression in regulatory Vα24JαQ T cells from identical twins discordant for type I diabetes

Wilson, S. Brian; Kent, Sally C.; Horton, Heidi F.; Hill, Andrew; Bollyky, Paul L.; Hafler, David A.; Strominger, Jack L.; Byrne, Michael C.

doi:10.1073/pnas.120161297

Cited by 108 publications

(92 citation statements)

References 33 publications

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“…The nonobese diabetic mouse has been found to be numerically and functionally deficient in NKT cells [10]. Furthermore a study of identical twins discordant for type 1 diabetes mellitus also showed differences in gene expression of NKT cells [11]. The NKT cells respond to α-galactosylceramide, a glycolipid, in the context of CD1d.…”

Section: Discussionmentioning

confidence: 99%

“…Studies have found NKT cell numbers to be reduced in type 1 diabetes mellitus [10,11], while activation of these cells by α-galactosylceramide prevents the onset of type 1 diabetes mellitus [12,13]. The relationship between NKT cells and CA seems to be different from the relationship between NKT cells and type 1 diabetes mellitus, since NKT K. Engkilde (*) .…”

Section: Introductionmentioning

confidence: 99%

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Inverse relationship between allergic contact dermatitis and type 1 diabetes mellitus: a retrospective clinic-based study

2006

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inverse relationship between allergic contact dermatitis and type 1 diabetes mellitus: a retrospective clinic-based study

2006

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“…This relationship between innate defense mechanisms and adaptive cellular phenomena was used to argue that CD1-restricted T cells function at the interface between innate and adaptive immunity (1)(2)(3)19). In rodents and humans, CD1d-restricted T cells seem to be dysfunctional in autoimmune-prone individuals and as a consequence, NOD mice would be predicted to have an impaired transition to appropriate adaptive responses (6,7). Despite this prediction, the exacerbation of diabetes by germ-line deletion of the CD1 locus suggests that CD1d-dependent events are impor- Fig.…”

Section: Discussionmentioning

confidence: 99%

Germ line deletion of the CD1 locus exacerbates diabetes in the NOD mouse

Shi

Flodström

Balasa

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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160

106

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Quantitative and qualitative defects in CD1-restricted natural killer T cells have been reported in several autoimmune-prone strains of mice, including the nonobese diabetic (NOD) mouse. These defects are believed to be associated with the emergence of spontaneous autoimmunity. Here we demonstrate that both CD1d-null NOD and CD1d-null NOD͞BDC2.5 T cell receptor transgenic mice have an accelerated onset and increased incidence of diabetes when compared with CD1d ؉/؊ and CD1d ؉/؉ littermates. The acceleration of disease did not seem to result from changes in the T helper (Th)1͞Th2 balance because lymphocytes purified from lymphoid organs and pancreatic islets of wild-type and CD1d-null mice secreted equivalent amounts of IFN-␥ and IL-4 after stimulation. In contrast, the pancreata of CD1d-null mice harbored significantly higher numbers of activated memory T cells expressing the chemokine receptor CCR4. Notably, the presence of these T cells was associated with immunohistochemical evidence of increased destructive insulitis. Thus, CD1d-restricted T cells are critically important for regulation of the spontaneous disease process in NOD mice.

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“…Furthermore, gene expression profiles of regulatory NKT cells from identical twins discordant for type I diabetes showed multiple differences [87].…”

Section: Type 1 Diabetesmentioning

confidence: 99%