Guo Liying, Wei Gang, Zhu Jinfang, Liao Wei, Leonard Warren J, Zhao Keji, Paul William
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Proc Natl Acad Sci U S A. 2009 Aug 11;106(32):13463-8. doi: 10.1073/pnas.0906988106. Epub 2009 Jul 29.
Expression of T1ST2, the IL-33R, by Th2 cells requires GATA3. Resting Th2 cells express little GATA3, which is increased by IL-33 and a STAT5 activator, in turn increasing T1ST2 from its low-level expression on resting Th2 cells. Th2 cells that have upregulated T1ST2 produce IL-13, but not IL-4, in response to IL-33 plus a STAT5 activator in an antigen-independent, NF-kappaB-dependent, cyclosporin A (CsA)-resistant manner. Similarly, Th17 cells produce IL-17A in response to IL-1beta and a STAT3 activator and Th1 cells produce IFNgamma in response to IL-18 and a STAT4 inducer. Thus, each effector Th cell produces cytokines without antigenic stimulation in response to an IL-1 family member and a specific STAT activator, implying an innate mechanism through which memory CD4 T cells are recruited by an induced cytokine environment.
Th2细胞表达IL-33受体T1ST2需要GATA3。静息Th2细胞表达的GATA3很少，IL-33和一种STAT5激活剂可使其增加，进而使静息Th2细胞上低水平表达的T1ST2增加。上调T1ST2的Th2细胞在抗原非依赖性、NF-κB依赖性、环孢素A（CsA）抗性的方式下，对IL-33加一种STAT5激活剂产生IL-13，但不产生IL-4。同样，Th17细胞对IL-1β和一种STAT3激活剂产生IL-17A，Th1细胞对IL-18和一种STAT4诱导剂产生IFNγ。因此，每种效应性Th细胞在无抗原刺激的情况下，对IL-1家族成员和特定的STAT激活剂产生细胞因子，这意味着一种先天机制，通过该机制记忆性CD4 T细胞被诱导的细胞因子环境招募。
