Stat4 is expressed in activated peripheral blood monocytes, dendritic cells, and macrophages at sites of Th1-mediated inflammation
Stat4 is expressed in activated peripheral blood monocytes, dendritic cells, and macrophages at sites of Th1-mediated inflammation
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DOI：
10.4049/jimmunol.164.9.4659
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发表时间：
2000-05-01
影响因子：
4.4
通讯作者：
O'Shea, JJ
中科院分区：
文献类型：
--
作者：
Frucht, DM;Aringer, M;O'Shea, JJ
Stat 4是参与促进细胞介导的免疫的关键转录因子，据报道其在成熟细胞中的表达仅限于T和NK细胞。然而，我们在这里证明，Stat 4的表达并不局限于淋巴细胞。在它们的基础状态下，单核细胞不表达Stat 4。然而，在活化时，IFN-γ和LPS处理的单核细胞和树突细胞表达高水平的Stat 4。人中单核细胞表达的Stat 4响应于IFN-α而不是IL-12被磷酸化。相反，Th 2细胞因子IL-4和IL-10特异性下调活化单核细胞中的Stat 4表达，而对Stat 6表达几乎没有影响。此外，从类风湿性关节炎患者获得的滑膜组织中的巨噬细胞在体内表达Stat 4，表明在原型Th 1介导的人类疾病中的潜在作用。人单核细胞中IFN-α诱导的Stat 4活化代表了Th 1炎症部位以前未识别的信号通路。
Stat4 is a key transcription factor involved in promoting cell-mediated immunity, whose expression in mature cells has been reported to be restricted to T and NK cells. We demonstrate here, however, that Stat4 expression is not restricted to lymphoid cells. In their basal state, monocytes do not express Stat4, Upon activation, however, IFN-gamma- and LPS-treated monocytes and dendritic cells express high levels of Stat4, Monocyte-expressed Stat4 in humans is phosphorylated in response to IFN-alpha, but not IL-12. In contrast, the Th2 cytokines, IL-4 and IL-10, specifically down-regulate Stat4 expression in activated monocytes, while having little effect on Stat6 expression. Moreover, macrophages in synovial tissue obtained from patients with rheumatoid arthritis express Stat4 in vivo, suggesting a potential role in a prototypical Th1-mediated human disease. IFN-alpha -induced Stat4 activation in human monocytes represents a previously unrecognized signaling pathway at sites of Th1 inflammation.