Peptide antagonism as a mechanism for NK cell activation.
作者： L. Fadda , G. Borhis , P. Ahmed , K. Cheent , S. V. Pageon
关键词:
摘要: Inhibition of natural killer (NK) cells is mediated by MHC class I receptors including the cell Ig-like receptor (KIR). We demonstrate that HLA-C binding peptides can function as altered peptide ligands for KIR and antagonize inhibition KIR2DL2/KIR2DL3. Antagonistic promote clustering at interface effector target cells, but do not result in NK cells. Our data show that, T small changes content regulate activity.
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