NFATc2 and NFATc3 transcription factors play a crucial role in suppression of CD4+ T lymphocytes by CD4+ CD25+ regulatory T cells.
NFATc2 and NFATc3 transcription factors play a crucial role in suppression of CD4+ T lymphocytes by CD4+ CD25+ regulatory T cells.
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DOI：
10.1084/jem.20041538
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发表时间：
2005-01-17
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NFATc2−/−c3−/−（双敲除[DKO]）小鼠的表型表明T细胞反应的失调调节，表现为大量淋巴结病、脾肿大和自身攻击现象。DKO小鼠的CD4+ CD25+ T细胞群缺乏调节能力，除了一小部分亚群高度表达糖皮质激素诱导的肿瘤坏死因子受体家族相关基因（GITR）和CD25。然而，无论是野生型还是DKO CD4+ CD25+调节性T细胞（T reg细胞）都不能抑制DKO CD4+ CD25−T辅助细胞的增殖。因此，NFATc2/c3联合缺乏与CD4+ CD25+ T细胞的发育是相容的，但使传统的CD4+ T细胞对抑制无反应，强调了NFAT蛋白对维持T细胞稳态的重要性。
The phenotype of NFATc2−/− c3−/− (double knockout [DKO]) mice implies a disturbed regulation of T cell responses, evidenced by massive lymphadenopathy, splenomegaly, and autoaggressive phenomena. The population of CD4+ CD25+ T cells from DKO mice lacks regulatory capacity, except a small subpopulation that highly expresses glucocorticoid-induced tumor necrosis factor receptor family–related gene (GITR) and CD25. However, neither wild-type nor DKO CD4+ CD25+ regulatory T cells (T reg cells) are able to suppress proliferation of DKO CD4+ CD25− T helper cells. Therefore, combined NFATc2/c3 deficiency is compatible with the development of CD4+ CD25+ T reg cells but renders conventional CD4+ T cells unresponsive to suppression, underlining the importance of NFAT proteins for sustaining T cell homeostasis.