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Gut‐Associated Lymphoid Tissues in Ulcerative Colitis
Author(s) -
Asakura Hitoshi,
Suzuki Azuma,
Ohtsuka Kazuo,
Hasegawa Katsuhiko,
Sugimura Kazuhito
Publication year - 1999
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/014860719902300507
Subject(s) - fas ligand , fas receptor , cd8 , ulcerative colitis , apoptosis , flow cytometry , immunology , lymphatic system , cd3 , cytotoxic t cell , biology , pathology , immune system , medicine , programmed cell death , in vitro , biochemistry , disease
Background: The main feature of ulcerative colitis (UC) is numerous infiltration of not only lymphocytes and plasma cells but also neutrophils and macrophages, indicating acute on chronic inflammation. Recent studies show that apoptosis may play an important role in the regulation of gut‐associated lymphoid tissues (GALT). Therefore, this study was performed to clarify apoptosis of lymphocytes in the peripheral blood and colonic mucosa of UC. Methods: Three‐color flow cytometry was used to clarify apoptosis of lymphocytes in the peripheral blood and colonic mucosa of patients with active and inactive UC compared with controls using fluorescence‐labeled monoclonal and polyclonal antibodies such as Fas (CD95), Fas ligand, CD4, CD8, CD45RO, etc. Results: The ratio of Fas and CD45RO double‐positive cells in the peripheral blood of UC patients was significantly increased in CD8 but not CD4 T cells when compared with controls. The ratio of Fas‐positive and CD45RO‐negative cells was significantly increased in CD4 and CD8 T cells of UC when compared with controls. There was unbalanced immunoregulation between CD4 and CD8 T cells in the colonic mucosa of UC probably due to apoptosis through Fas‐Fas ligand system. Conclusions: Abnormal GALT system was found in UC probably due to dysregulation of T cells through Fas‐Fas ligand system. (Journal of Parenteral and Enteral Nutrition23:S25‐S28, 1999)