FAS-INDEPENDENT APOPTOSIS OF T-CELLS VIA KILLER-CELL INHIBITORY RECEPTORS

Killer cell inhibitory receptor (KIR) is expressed on NK cells and T c ells, and negatively regulates the recognition of these cells via its binding to HLA class I molecules, Here we show the evidence that KIR i s involved in apoptosis of T cells, The triggering of NKB1 molecules u sing DX9 anti-NKB1 mAb induced apoptosis of the cytotoxic T lymphocyte (CTL) clone expressing NKB1. Moreover, the cross-linking of NKB1 mole cules together with CD3 molecules enhanced the apoptosis. The CTL clon e carries Fas molecules, but failed to express Fas ligand (FasL) even after the cross-linking of both NKB1 and CD3 molecules. The apoptosis of the CTL clone induced by the cross-linking of both NKB1 and CD3 mol ecules was inhibited by IL-1 beta-converting enzyme (ICE) inhibitor. T hese results together indicate that the apoptosis of CTL induced by th e triggering of NKB1 molecules is not Fas-mediated but is linked to ot her signaling pathways using the ICE-like protease cascade.