Cutting edge:: TNFR-Shedding by CD4+CD25+ regulatory T cells inhibits the induction of inflammatory mediators
Cutting edge:: TNFR-Shedding by CD4+CD25+ regulatory T cells inhibits the induction of inflammatory mediators
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DOI：
10.4049/jimmunol.180.5.2747
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发表时间：
2008-03-01
影响因子：
4.4
通讯作者：
Toes, Rene E. M.
中科院分区：
文献类型：
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作者：
van Mierlo, Geertje J. D.;Scherer, Hans U.;Toes, Rene E. M.
CD 4（+）CD 25（+）调节性T（Treg）细胞在维持对自身和非自身的耐受中起重要作用。在几种T细胞介导的（自身）免疫模型中，Treg细胞通过抑制致病性T细胞应答发挥保护作用。此外，Treg细胞可以调节T细胞非依赖性炎症。我们现在发现，CD 4（+）CD 25（+）Treg细胞能够释放大量TNFRII。这是由它们在体外和体内抑制TNF-α作用的能力证实的。在体内，Treg细胞抑制小鼠中响应于LPS注射的IL-6产生。相反，来自TNFRII缺陷小鼠的Treg细胞不能这样做，尽管它们在常规体外抑制测定中抑制T细胞增殖的能力不受阻碍。因此，TNFRII的脱落代表了一种新的机制，通过该机制Treg细胞可以抑制TNT的作用，TNT是一种驱动炎症的关键细胞因子。
CD4(+) CD25(+) regulatory T(Treg) cells play an essential role in maintaining tolerance to self and nonself. In several models of T cell-mediated (auto) immunity, Treg cells exert protective effects by the inhibition of pathogenic T cell responses. In addition, Treg cells can modulate T cell-independent inflammation. We now show that CD4(+)CD25(+) Treg cells are able to shed large amounts of TNFRII. This is paralleled by their ability to inhibit the action of TNF-alpha both in vitro and in vivo. In vivo, Treg cells suppressed IL-6 production in response to LPS injection in mice. In contrast, Treg cells from TNFRII-deficient mice were unable to do so despite their unhampered capacity to suppress T cell proliferation in a conventional in vitro suppression assay. Thus, shedding of TNFRII represents a novel mechanism by which Treg cells can inhibit the action of TNT, a pivotal cytokine driving inflammation.