Altered Patterns of Secretion of IgA and IgG Subclasses by Ulcerative Colitis and Crohn’s Disease Intestinal Mononuclear Cells
Ulcerative colitis (UC) and Crohn’s disease (CD) are inflammatory bowel diseases (IBD) due to unknown etiologic and potentiating factors resulting in immune responses of a chronic inflammatory nature (1). There is an increase in cytoplasmic, surface, and secreted antibodies from IBD intestinal lymphocytes, due mainly to enhanced expression and production of IgG (2–4). In previous studies (5,6) we have found that immunoglobulin secretion patterns by peripheral blood and intestinal mononuclear cells (MNC) from inflammatory bowel disease patients is altered. IBD peripheral blood MNC reveal a markedly increased spontaneous secretion of IgA which is partially suppressed by PWM (5,6). Intestinal MNC from control specimens also spontaneously secrete large amounts of IgA, which is suppressed by PWM (5,6). In IBD patients, intestinal MNC exhibit decreased spontaneous IgA secretion, but have increased IgG secretion compared with control intestinal MNC (5–7). The changes in antibody secretion observed in IBD could be due to: (a) preferential proliferation of subpopulations of cells due to immunoregulatory alteration; (b) switching of the isotype and/or subclass of antibody secreted by the lymphocytes themselves; or (c) changes in the homing and trafficking patterns of the lymphocytes due to the inflammatory process.
KeywordsHPLC Glycerol Albumin Adenocarcinoma Myeloma
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