作者: R. P. MacDermott , G. S. Nash , M. G. Scott , M. H. Nahm , M. J. Bertovich
DOI: 10.1007/978-1-4684-5344-7_38
关键词:
摘要: Ulcerative colitis (UC) and Crohn’s disease (CD) are inflammatory bowel diseases (IBD) due to unknown etiologic potentiating factors resulting in immune responses of a chronic nature (1). There is an increase cytoplasmic, surface, secreted antibodies from IBD intestinal lymphocytes, mainly enhanced expression production IgG (2–4). In previous studies (5,6) we have found that immunoglobulin secretion patterns by peripheral blood mononuclear cells (MNC) patients altered. MNC reveal markedly increased spontaneous IgA which partially suppressed PWM (5,6). Intestinal control specimens also spontaneously secrete large amounts IgA, patients, exhibit decreased secretion, but compared with (5–7). The changes antibody observed could be to: (a) preferential proliferation subpopulations immunoregulatory alteration; (b) switching the isotype and/or subclass lymphocytes themselves; or (c) homing trafficking process.