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Alterations of immuno globulin m immuno globulin g and immuno globulin a synthesis and secretion by peripheral blood and intestinal mononuclear cells from patients with ulcerative colitis and crohns disease



Alterations of immuno globulin m immuno globulin g and immuno globulin a synthesis and secretion by peripheral blood and intestinal mononuclear cells from patients with ulcerative colitis and crohns disease



Gastroenterology 81(5): 844-852



During 12 days in vitro culture, synthesis and secretion of IgM, IgG and IgA was examined by isolated intestinal mononuclear cells from normal subjects, and from patients with ulcerative colitis and Crohn's disease as well as by peripheral blood mononuclear cells from patients with ulcerative colitis. Crohn's disease and systemic lupus erythematosus. In comparison with normal peripheral blood mononuclear cells, normal intestinal mononuclear cells exhibited moderately increased spontaneous secretion of IgG and IgM and markedly increased spontaneous secretion of IgA. In contrast (when compared with normal intestinal momononuclear cells), Crohn's disease and ulcerative colitis intestinal mononuclear cells exhibited decreases spontaneous antibody secretion. Pokeweed mitogen stimulation resulted in only moderate or no increase in antibody secretion. Investigation of 3H-thymidine incorporation revealed completely normal patients with low spontaneous blast transformation by all intestinal mononuclear cell populations and a marked increase after pokeweed mitogen stimulation. Examination of antibody secretion by peripheral blood mononuclear cells from active, untreated patients with ulcerative colitis, Crohn's disease and systemic lupus erythematosus revealed that all exhibited similar patterns as follows: moderately increased spontaneous synthesis and secretion of IgG and IgM, and markedly increased synthesis and secretion of IgA by unstimulated mononuclear cells over 12 days. Stimulation with pokeweed mitogen resulted in little or no increase and, in some instances, suppression of antibody secretion. In all instances, the predominant antibody produced was IgA, which was spontaneously secreted in greater amounts than IgG or IgM. There are 2 possible explanations for these results. The 1st is that IgA precursor cells are in a highly activated state in normal intestinal lamina propria and because of intestinal inflammation migrate from the intestine into the peripheral blood in increased numbers. The alternative explanation is that a primary mucosal immunodeficiency is present in the intestines of inflammatory bowel disease patients, thus allowing agents to penetrate the intestinal mucosal and subsequently initiate a local inflammation and a heightened systemic immune response. In either case, patients with ulcerative colitis and Crohn's disease revidently exhibit major alterations of in vitro synthesis and secretion of Ig in general and IgA in particular.

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