Genetic Dissection of Vα14Jα18 Natural T Cell Number and Function in Autoimmune-Prone Mice
作者： Naoto Matsuki , Aleksandar K. Stanic , Monica E. Embers , Luc Van Kaer , Laurence Morel
DOI: 10.4049/JIMMUNOL.170.11.5429
关键词:
摘要: Nonobese diabetic (NOD) mice, a model for type I diabetes (TID), have reduced numbers of invariant Vα14Jα18 TCR α-chain-positive natural T (iNKT) cells that do not release IL-4 in response to vivo activation through their Ag receptor. The deficit iNKT cell number and function is implicated immune dysregulation the etiology TID. Therefore, we reasoned genetic determinant(s) controls might lie within Idd (insulin-dependent susceptibility locus) regions, which are known contain TID resistance or genes. A systematic analysis congenic mice revealed neither nor inability rapidly secrete acute by underlies mechanism protection from mice. Moreover, regulation appears be under control several most notable these map Idd4 , Idd5 Idd9.1 Idd13 regions mouse genome. Together findings provide clue mechanism(s) underlying deficiency NOD
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