Peripheral blood mononuclear cells from patients with inflammatory bowel disease exhibit normal function in the allogeneic and autologous mixed leukocyte reaction and cell-mediated lympholysis.

We have examined the T-cell functional capabilities of peripheral blood mononuclear cells from 32 active or inactive patients with ulcerative colitis and Crohn's disease by examining blastogenic responsiveness in the allogeneic and autologous mixed leukocyte reaction and cytotoxic capabilities in cell-mediated lympholysis. Severely ill, malnourished, or preoperative patients, or patients being treated with greater than 10 mg of prednisone per day were excluded from study. Studies using the allogeneic mixed leukocyte reaction revealed no decreased responsiveness by inflammatory bowel disease peripheral blood cells. In cell-mediated lympholysis, healthy control peripheral blood mononuclear cells exhibited 17% cytotoxicity, and there was no significant difference in killing exhibited by patients with inflammatory bowel disease. In study of the autologous mixed leukocyte reaction, cells were separated using techniques that included exposure to xenoantigens (fetal calf serum and sheep red blood cells), and peripheral blood cells from inflammatory bowel disease patients did not exhibit major defects in responsiveness. Therefore, in these experiments, we have detected no significant depression in three major T-cell functions by peripheral blood cells in moderately ill patients with ulcerative colitis or Crohn's disease. We conclude that defects in these capabilities may not be primarily causative in the immunopathogenesis of inflammatory bowel disease or the increased incidence of cancer seen in ulcerative colitis. Instead, when defects in these T-cell functions are observed, they may be influenced by the techniques used or may represent secondary in vitro immunologic events related to disease severity, inflammation, medications, or other causes that are not specific for inflammatory bowel disease.