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pubmed-article:18417224pubmed:abstractTextInterleukin-2 (IL-2) plays an established role in T-cell regulation through binding to the high-affinity IL-2 receptor (IL-2R). The alpha-chain encoded by the IL2RA (CD25) gene is a substantial component of the high-affinity receptor molecule highly expressed by activated T lymphocytes. Recently, a strong evidence was obtained for the involvement of IL-2RA in conferring susceptibility to type 1 diabetes (T1D). Significant association with T1D was also found in the region on chromosome 4q27 containing the IL2 gene and homologous to the susceptibility locus idd3 in non-obese diabetic (NOD) mice, an animal model for human T1D. Here we focus on the discussion of these new findings suggesting for a crucial role of IL-2/IL-2RA-mediated regulatory mechanisms in preventing T1D. The non-redundant role of IL-2 and its receptor in etiology of T1D could be particularly attributable to the regulation of CD4+ CD25+ regulatory T cells, whose function is critical in maintaining immune homeostasis.lld:pubmed
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pubmed-article:18417224pubmed:year2008lld:pubmed
pubmed-article:18417224pubmed:articleTitleThe crucial role of IL-2/IL-2RA-mediated immune regulation in the pathogenesis of type 1 diabetes, an evidence coming from genetic and animal model studies.lld:pubmed
pubmed-article:18417224pubmed:affiliationDepartment of Pathology, University of Pittsburgh Medical Center, A719 Scaife Hall, Pittsburgh, PA 15261, USA. dimitry.chistiakov@eudoramail.comlld:pubmed
pubmed-article:18417224pubmed:publicationTypeJournal Articlelld:pubmed
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