CD83 刺激的单核细胞通过产生前列腺素 E2 来抑制 T 细胞免疫应答。
CD83-stimulated monocytes suppress T-cell immune responses through production of prostaglandin E2.
机构信息
Institute of Medical Biotechnology and Jiangsu Stem Cell Key Laboratory, Soochow University, Suzhou 215007, China.
出版信息
Proc Natl Acad Sci U S A. 2011 Nov 15;108(46):18778-83. doi: 10.1073/pnas.1018994108. Epub 2011 Nov 7.
CD83 is commonly known as a specific marker for mature dendritic cells. It has been shown to be important for CD4(+) T-cell development in the thymus. However, its function in the peripheral immune system remains enigmatic. Here, we show that CD83 inhibits proliferation and production of IL-2 and IFN-γ by T cells, and the inhibitory effect of CD83 is mediated by monocytes. Prostaglandin E2 (PGE(2)), but not IL-10 or TGF-β, was up-regulated specifically by CD83 in monocytes. Consistent with high levels of PGE(2), expression of COX-2 also was increased upon CD83 treatment. NF-κB activation also is required for induction of PGE(2) by CD83. Finally, application of the COX-2-selective inhibitor NS-398 fully prevented CD83-triggered inhibition of T-cell responses. Our study establishes an immune-regulatory mechanism by CD83 via stimulation of PGE(2) production in monocytes.
CD83 通常被认为是成熟树突状细胞的特异性标志物。它已被证明对胸腺中 CD4(+) T 细胞的发育很重要。然而，其在外周免疫系统中的功能仍然是个谜。在这里，我们表明 CD83 抑制 T 细胞的增殖和 IL-2 和 IFN-γ 的产生，而 CD83 的抑制作用是由单核细胞介导的。前列腺素 E2（PGE(2)），而不是 IL-10 或 TGF-β，是由 CD83 在单核细胞中特异性上调的。与 PGE(2) 水平升高一致，COX-2 的表达也在 CD83 处理后增加。NF-κB 的激活也需要诱导 COX-2 来产生 PGE(2)。最后，应用 COX-2 选择性抑制剂 NS-398 可完全阻止 CD83 触发的 T 细胞反应的抑制。我们的研究通过 CD83 在单核细胞中刺激 PGE(2)的产生，建立了一种免疫调节机制。
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