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Monochloramine enhances Fas (APO‐1/CD95)‐induced apoptosis in Jurkat T cells

Monochloramine derivatives are physiological oxidants produced by activated neutrophils. We report the effects of chemically prepared monochloramine (NH2Cl) on Fas‐induced apoptosis in Jurkat T cells. When the cells were pretreated with NH2Cl (20–70 μM), subsequent addition of apoptosis‐inducing anti‐Fas antibody resulted in a synergistic enhancement of apoptosis. Treatment of NH2Cl (50–70 μM) alone resulted in a slight but definite apoptosis. Caspase activities, as measured by DEVD and IETD cleavage activities, were also elevated synergistically by NH2Cl + anti‐Fas antibody stimulation. Moreover, a broad caspase inhibitor, Z‐VAD‐fmk, almost completely inhibited the apoptosis induced by NH2Cl and/or anti‐Fas antibody. Fas expression on the Jurkat cell surface was not affected by the NH2Cl treatment. After 3 h of NH2Cl treatment, when the apoptosis was beginning to increase, the cells showed cytochrome c release from mitochondria, proteolytic activation of caspase 9, and poly (ADP‐ribose) polymerase cleavage, regardless of Fas stimulation. Z‐VAD‐fmk almost completely inhibited this poly (ADP‐ribose) polymerase cleavage, but not cytochrome c release. By contrast, Fas stimulation alone resulted in neither cytochrome c release nor caspase 9 activation at 3 h, and the increase in the DEVD cleavage activity and apoptosis became evident at later time points. These results suggested that NH2Cl enhanced Fas‐induced apoptosis through the cytochrome c release and caspase 9 activation at the early stage of apoptosis. Chloramines derived from acute inflammation may modify immune reactions, such as cell‐mediated cytotoxicity and some autoimmune diseases, by the enhancement of Fas‐induced apoptosis. J. Leukoc. Biol. 67: 46–52; 2000.