Effects of Peptide on NK cell-mediated MHC I recognition.
Effects of Peptide on NK cell-mediated MHC I recognition.
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DOI：
10.3389/fimmu.2014.00133
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发表时间：
2014
影响因子：
7.3
通讯作者：
Khakoo SI
中科院分区：
文献类型：
--
作者：
Cassidy SA;Cheent KS;Khakoo SI
MHC I类抑制性受体在控制自然杀伤（NK）细胞活性中具有核心作用。在他们发现后不久，人们发现这些受体具有一定程度的肽选择性。这种肽的选择性已被证明为所有抑制性杀伤细胞免疫球蛋白样受体（KIR）测试的日期，某些活化KIR，以及C型凝集素样受体家族的成员。这种选择性比T细胞受体的肽特异性广泛得多，NK细胞受体识别肽基序，而不是单个肽。NK细胞上的抑制性受体可以检测靶细胞表面上表达的肽：MHC复合物，因此抑制性信号的后续转导取决于这些MHC I类复合物的总肽含量。在功能上，表达KIR的NK细胞已经显示出对MHC I类的肽含量的变化出乎意料地敏感，因为弱接合KIR的肽：MHC I类复合物可以拮抗由更强的KIR结合肽：MHC I类复合物的接合产生的抑制信号。这种特性为表达KIR的NK细胞提供了识别肽：MHC I类库变化的潜力，这可能发生在病毒感染和肿瘤发生期间。相比之下，在存在HLA I类前导肽的情况下，病毒衍生肽可以通过在不存在NKG2A的情况下募集CD94来诱导对表达CD94：NKG2A的NK细胞的协同抑制。另一方面，CD94：NKG2A阳性NK细胞对MHC I类分子水平的变化非常敏感。肽拮抗作用和对MHC I类水平变化的敏感性是区分KIR和CD94：NKG2A的特性。表达这些受体的NK细胞性质的细微差异为具有针对MHC I类的互补抑制性受体系统提供了理论基础。
The inhibitory receptors for MHC class I have a central role in controlling natural killer (NK) cell activity. Soon after their discovery, it was found that these receptors have a degree of peptide selectivity. Such peptide selectivity has been demonstrated for all inhibitory killer cell immunoglobulin-like receptor (KIR) tested to date, certain activating KIR, and also members of the C-type lectin-like family of receptors. This selectivity is much broader than the peptide specificity of T cell receptors, with NK cell receptors recognizing peptide motifs, rather than individual peptides. Inhibitory receptors on NK cells can survey the peptide:MHC complexes expressed on the surface of target cells, therefore subsequent transduction of an inhibitory signal depends on the overall peptide content of these MHC class I complexes. Functionally, KIR-expressing NK cells have been shown to be unexpectedly sensitive to changes in the peptide content of MHC class I, as peptide:MHC class I complexes that weakly engage KIR can antagonize the inhibitory signals generated by engagement of stronger KIR-binding peptide:MHC class I complexes. This property provides KIR-expressing NK cells with the potential to recognize changes in the peptide:MHC class I repertoire, which may occur during viral infections and tumorigenesis. By contrast, in the presence of HLA class I leader peptides, virus-derived peptides can induce a synergistic inhibition of CD94:NKG2A-expressing NK cells through recruitment of CD94 in the absence of NKG2A. On the other hand, CD94:NKG2A-positive NK cells can be exquisitely sensitive to changes in the levels of MHC class I. Peptide antagonism and sensitivity to changes in MHC class I levels are properties that distinguish KIR and CD94:NKG2A. The subtle difference in the properties of NK cells expressing these receptors provides a rationale for having complementary inhibitory receptor systems for MHC class I.
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发表时间：
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期刊：
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影响因子：
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