Deficient cell-mediated cytotoxicity and hyporesponsiveness to interferon and mitogenic lectin activation by inflammatory bowel disease peripheral blood and intestinal mononuclear cells.

Intestinal mononuclear cells are poor mediators of spontaneous and antibody-dependent cellular cytotoxicity. In this study, we found that both interferon and mitogenic lectins were able to induce increased levels of cell-mediated cytotoxicity by intestinal mononuclear cells. Intestinal mononuclear cells from patients with inflammatory bowel disease exhibited hyporesponsiveness to cytotoxic activation by interferon or lectins compared with control intestinal mononuclear cells. Peripheral blood mononuclear cells from patients with Crohn's disease exhibited deficient spontaneous and antibody-dependent cytotoxicity that could be partially reversed by interferon or mitogenic lectins. These studies demonstrate that exogenous agents or endogenous factors can induce deficient intestinal and peripheral blood cytotoxic effector cells from inflammatory bowel disease patients to become active. In comparison with control cells, however, intestinal and peripheral blood mononuclear cells from inflammatory bowel disease patients are not only deficient in cytotoxic capabilities but also are hyporesponsive to interferon and lectin activation.