Functional expression of CD134 by neutrophils

Functional expression of CD134 by neutrophils
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DOI:
10.1002/eji.200424863
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发表时间:
2004-08-01
影响因子:
5.4
通讯作者:
Simon, HU
Simon, HU
中科院分区:
医学3区
文献类型:
--
作者:
Baumann, R;Yousefi, S;Simon, HU

文献摘要

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CD 134(OX 40)是在活化的T细胞上表达的肿瘤坏死因子(TNF)受体超家族的成员。在这里,我们表明,人外周血中性粒细胞表达CD 134。通过可溶性CD 134配体(OX 40配体/gp 34)激活CD 134导致延迟的半胱天冬酶-3激活,并因此导致延迟的体外中性粒细胞凋亡。此外,CD 134配体,如G-CSF,维持抗凋亡Mcl-1水平,并抑制这些细胞中促凋亡Bcl-2家族成员Bid和Bax的裂解,表明CD 134介导的信号阻断线粒体激活附近的凋亡途径。总之,CD 134调节中性粒细胞存活,表明该分子不仅有助于适应性免疫应答,而且有助于先天性免疫应答。
CD134 (OX40) is a member of the tumor necrosis factor (TNF) receptor superfamily expressed on activated T cells. Here, we show that human peripheral blood neutrophils express CD134. Activation of CD134 by soluble CD134 ligand (OX40 ligand/gp34) resulted in delayed caspase-3 activation and consequently in delayed neutrophil apoptosis in vitro. Moreover, CD134 ligand,like G-CSF, maintained anti-apoptotic Mcl-1 levels and inhibited cleavage of the pro-apoptotic Bcl-2 family members Bid and Bax in these cells, suggesting that CD134-mediated signals block apoptosis pathways proximal to mitochondria activation. In conclusion, CD134 regulates neutrophil survival, suggesting that this molecule does not only contribute to adaptive but also to innate immune responses.