Venuprasad K, Chattopadhyay Subhasis, Saha Bhaskar
National Centre for Cell Science, Ganeshkhind, Pune, India.
Hum Immunol. 2003 Jan;64(1):38-43. doi: 10.1016/s0198-8859(02)00689-4.
We previously reported that human peripheral blood neutrophils express CD28 and interact with macrophage B7 to generate CD28 signaling through PI-3 kinase. Here, we demonstrate that crosslinking of CD28 on neutrophils results in the release of IFN-gamma, which restricts amastigote growth and modulates CD4+ T cells cytokine secretion. CD28 crosslinking also induces a T-cell chemotactic factor (TCF) that induces chemotactic migration of CD4+ T cells. Based on our previous and the current set of data, we propose an operational model explaining how neutrophils are involved in Leishmania infection and how the reported effect of neutrophils on the control of infection is mediated by alteration of T-cell function.
我们之前报道过,人类外周血中性粒细胞表达CD28,并与巨噬细胞B7相互作用,通过PI-3激酶产生CD28信号。在此,我们证明中性粒细胞上CD28的交联导致IFN-γ的释放,这限制了无鞭毛体的生长并调节CD4+ T细胞细胞因子的分泌。CD28交联还诱导一种T细胞趋化因子(TCF),该因子诱导CD4+ T细胞的趋化迁移。基于我们之前和当前的一系列数据,我们提出了一个操作模型,解释中性粒细胞如何参与利什曼原虫感染,以及中性粒细胞对感染控制的报道效应是如何通过T细胞功能的改变介导的。