Runt-related transcription factor 3 is involved in the altered phenotype and function in ThPok-deficient invariant natural killer T cells
Runt-related transcription factor 3 is involved in the altered phenotype and function in ThPok-deficient invariant natural killer T cells作者机构：Institute of Immunology Zhejiang University School of Medicine Hangzhou China
出 版 物：《Cellular & Molecular Immunology》 (中国免疫学杂志（英文版）)
年 卷 期：2014年第11卷第3期
页 面：232-244页
核心收录：
学科分类：090603[农学-临床兽医学] 0710[理学-生物学] 07[理学] 09[农学] 0906[农学-兽医学] 071007[理学-遗传学]
基 金：国家自然科学基金 the National Basic Research Program of China (973 Program and 863 Program) 浙江省自然科学基金 国家教育部高等学校博士学科点专项科研基金 the Fundamental Research Funds for the Central Universities
主 题：α-galactosylceramide iNKT cells liver Runx3 ThPok
摘 要：The interplay between the CD4-1ineage transcription factor ThPok and the CD8-iineage transcription factor, runt-related transcription factor 3 （Runx3）, in T-cell development has been extensively documented. However, little is known about the roles of these transcription factors in invariant natural killer T （iNKT） cell development. CDld-restricted iNKT cells are committed to the CD4＋CD8- and CD4-CD8- sublineages, which respond to antigen stimulation with rapid and potent release of T helper （Th） 1 and Th2 cytokines. However, previous reports have demonstrated a new population of CD8~ NKT cells in ThPok-deficient mice. In the current study, we sought to determine whether Runx3 was involved in the re-expression of CD8 and function of iNKT cells in the absence of ThPok. We used mice lacking Runx3, ThPok or both and verified that Runx3 was partially responsible for the appearance of CD8^＋ iNKT cells in ThPok knockout mice. Additionally, Runx3 participated in the immune response mediated by iNKT cells in a model of α-galactosylceramide-induced acute hepatitis. These results indicate that Runx3 is crucial for the phenotypic and functional changes observed in ThPok-deficient iNKT cells.
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