Mechanisms of NK cell recognition of SIV-infected CD4+ T cells

NK细胞识别SIV感染的CD4 T细胞的机制

• 批准号: 182848482
• 负责人: Dr. Henoch Sangjoon Hong
• 金额: --
• 依托单位: Immunology Program
• 依托单位国家: 德国
• 项目类别: Research Fellowships
• 财政年份: 2010
• 资助国家: 德国
• 起止时间: 2009-12-31 至 2012-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/182848482?language=en
• 关键词: Mechanisms; NK; cell; recognition; SIV

NK cells recognize virus-infected cells by integrating the sum of signals transduced by activating and inhibitory NK receptors. NKG2D is a well-described activating receptor. Previous studies examining recognition of HIV-infected CD4+ T cells have implicated modulation of NKG2D ligands by HIV proteins. In addition, modulation of inhibitory pathways has also been reported. However, while NK cells have been previously reported to recognize SIV-infected cells, virtually nothing is known about the specific mechanisms responsible for this interaction. We will examine recognition of autologous SIV-infected CD4+ T cells by macaque NK cells to determine the relative contributions of MHC class I downregulation and NKG2D ligand upregulation, and the specific SIV proteins that mediate these effects.

NK细胞通过整合由活化和抑制性NK受体转导的信号的总和来识别病毒感染的细胞。NKG2D是一种已充分描述的活化受体。先前检查HIV感染的CD4+ T细胞识别的研究涉及HIV蛋白对NKG2D配体的调节。此外，还报道了抑制途径的调节。然而，虽然NK细胞以前曾被报道识别SIV感染的细胞，但实际上对这种相互作用的具体机制一无所知。我们将研究猕猴NK细胞对自体SIV感染的CD4+ T细胞的识别，以确定MHC I类下调和NKG2D配体上调的相对贡献，以及介导这些效应的特异性SIV蛋白。