Abromson-Leeman Sara, Bronson Roderick T, Dorf Martin E
Dept. of Pathology, Harvard Medical School, Boston, MA 02115, USA.
J Neuroimmunol. 2009 Oct 30;215(1-2):10-24. doi: 10.1016/j.jneuroim.2009.07.007. Epub 2009 Aug 18.
Th1/Th17 cells, secreting both IFNgamma and IL-17, are often associated with inflammatory pathology. We cloned and studied the cytokine phenotypes of MBP-specific, TCR-identical encephalitogenic CD4+ cells in relationship to Th1- and Th17-associated transcription factors T-bet and RORgammat. IFNgamma-producing cells could be sub-divided into those that are T-bet(+)/RORgammat(-) and those that are T-bet(+)/RORgammat(+). The latter comprises a spectrum of phenotypes, as defined by IL-17 production, and can be induced to up-regulate IL-23R with IL-12 or IL-23. The former, bona fide Th1 cells, lack IL-23R expression under all conditions. In vivo, T-bet(+)/RORgammat(-) and T-bet(+)/RORgammat(+) clones induce EAE equally well.
分泌干扰素γ（IFNγ）和白细胞介素-17（IL-17）的Th1/Th17细胞通常与炎症病理相关。我们克隆并研究了与髓鞘碱性蛋白（MBP）特异性、T细胞受体（TCR）相同的致脑炎性CD4 +细胞的细胞因子表型，以及与Th1和Th17相关的转录因子T-bet和维甲酸相关孤儿受体γt（RORγt）的关系。产生IFNγ的细胞可细分为T-bet(+)/RORγt(-)细胞和T-bet(+)/RORγt(+)细胞。后者包含一系列由IL-17产生所定义的表型，并且可以被IL-12或IL-23诱导上调IL-23受体（IL-23R）的表达。前者，即真正的Th1细胞，在所有条件下均缺乏IL-23R表达。在体内，T-bet(+)/RORγt(-)和T-bet(+)/RORγt(+)克隆诱导实验性自身免疫性脑脊髓炎（EAE）的效果相同。
