肽拮抗作用作为自然杀伤细胞激活的一种机制。
Peptide antagonism as a mechanism for NK cell activation.
作者信息
Fadda Lena, Borhis Gwenoline, Ahmed Parvin, Cheent Kuldeep, Pageon Sophie V, Cazaly Angelica, Stathopoulos Stavros, Middleton Derek, Mulder Arend, Claas Frans H J, Elliott Tim, Davis Daniel M, Purbhoo Marco A, Khakoo Salim I
机构信息
Divisions of Medicine and Cell and Molecular Medicine, Imperial College London, London W2 1PG, United Kingdom.
出版信息
Proc Natl Acad Sci U S A. 2010 Jun 1;107(22):10160-5. doi: 10.1073/pnas.0913745107. Epub 2010 May 3.
Abstract
Inhibition of natural killer (NK) cells is mediated by MHC class I receptors including the killer cell Ig-like receptor (KIR). We demonstrate that HLA-C binding peptides can function as altered peptide ligands for KIR and antagonize the inhibition mediated by KIR2DL2/KIR2DL3. Antagonistic peptides promote clustering of KIR at the interface of effector and target cells, but do not result in inhibition of NK cells. Our data show that, as for T cells, small changes in the peptide content of MHC class I can regulate NK cell activity.
摘要
自然杀伤（NK）细胞的抑制作用由包括杀伤细胞免疫球蛋白样受体（KIR）在内的MHC I类受体介导。我们证明，HLA - C结合肽可作为KIR的改变肽配体，并拮抗由KIR2DL2/KIR2DL3介导的抑制作用。拮抗肽促进KIR在效应细胞和靶细胞界面处聚集，但不会导致NK细胞的抑制。我们的数据表明，与T细胞一样，MHC I类肽含量的微小变化可调节NK细胞活性。
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