首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Inhibitory Killer Immunoglobulin-like receptors to self HLA-B and HLA-C ligands contribute differentially to Natural Killer cell functional potential in HIV infected slow progressors
【24h】

Inhibitory Killer Immunoglobulin-like receptors to self HLA-B and HLA-C ligands contribute differentially to Natural Killer cell functional potential in HIV infected slow progressors

机译:HLA-B和HLA-C自身配体的抑制性杀手免疫球蛋白样受体在感染HIV的缓慢进展者中对自然杀伤细胞功能潜力的贡献不同

获取原文
获取原文并翻译 | 示例
           

摘要

Inhibitory Killer Immunoglobulin-like Receptors (iKIR) interact with their ligands, HLA molecules, to license Natural Killer (NK) cells for functional competence. Previous studies stimulating peripheral blood mononuclear cells (PBMCs) with the HLA-devoid K562 cell line revealed that NK cells from individuals with an iKIR encoded by the KIR3DL1 locus with self HLA-Bw4 as their ligands, had higher frequencies of tri-functional NK cells that expressed the degranulation marker CD107a and secreted Interferon-γ and Tumor Necrosis Factor-α than those from individuals who were homozygous for HLA-Bw6 alleles, which are not ligands for these iKIR. To assess the effect of other iKIR to self-HLA (S-iKIR) on the NK cell response, we compared HIV-infected slow progressors (SP) carrying S-iKIR to HLA-C alleles with or without S-iKIR to HLA-Bw4. We show that S-iKIR to HLA-B and C alleles differ in their contribution to NK cell functional potential in HIV-infected SP upon stimulation with K562 targets.
机译:抑制性杀手免疫球蛋白样受体(iKIR)与它们的配体HLA分子相互作用,以使自然杀手(NK)细胞具有功能能力。先前使用不含HLA的K562细胞系刺激外周血单个核细胞(PBMC)的研究表明,来自以iKIR编码的KIR3DL1基因座的个体,其自身HLA-Bw4作为配体的NK细胞具有较高的三功能NK细胞频率与那些不是这些iKIR配体的HLA-Bw6等位基因纯合子的个体相比,它们表达了脱粒标记物CD107a并分泌了干扰素-γ和肿瘤坏死因子-α。为了评估其他iKIR对自身HLA(S-iKIR)对NK细胞反应的影响,我们比较了携带S-iKIR的HIV感染的慢进程(SP)与有或没有S-iKIR的HLA-C等位基因对HLA- Bw4。我们显示S-iKIR到HLA-B和C等位基因在K562靶点刺激后对HIV感染的SP中NK细胞功能潜能的贡献不同。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号