title: Crucial role for CD69 in the pathogenesis of dextran sulphate sodium-induced colitis.
abstract: CD69 is a membrane molecule transiently expressed on activated lymphocytes, and its selective expression in inflammatory infiltrates suggests that it plays a role in the pathogenesis of inflammatory diseases. In this study, we used CD69-deficient (CD69 KO) mice to assess the role of CD69 in the pathogenesis of dextran sulphate sodium (DSS)-induced acute and chronic colitis. The severity of colitis was assessed by the survival rate, clinical signs, colon length, histological examination and the expression of cytokines and chemokines in the large intestines. Both acute and chronic colitis were attenuated in the CD69 KO mice, as reflected by the lower lethality, weight loss, clinical signs, and improved histological findings. CD69(+) cells infiltrated extensively into the inflamed mucosa of the colon in WT mice after DSS treatment. Experiments with the transfer of WT CD4 T cells into CD69 KO mice restored the induction of colitis. The administration of an anti-CD69 antibody also inhibited the induction of the DSS-induced colitis. These results indicate that CD69 expressed on CD4 T cells plays an important role in the pathogenesis of DSS-induced acute and chronic colitis, and that CD69 could be a possible therapeutic target for colitis.
authors.affiliation: Department of Microbiology and Immunology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
authors.forename: Akihiro
authors.initials: A
authors.lastname: Hasegawa
authors.forename: Chiaki
authors.initials: C
authors.lastname: Iwamura
authors.forename: Masayuki
authors.initials: M
authors.lastname: Kitajima
authors.forename: Kahoko
authors.initials: K
authors.lastname: Hashimoto
authors.forename: Ken-Ichiro
authors.initials: K
authors.lastname: Otsuyama
authors.forename: Hidetaka
authors.initials: H
authors.lastname: Ogino
authors.forename: Toshinori
authors.initials: T
authors.lastname: Nakayama
authors.forename: Mutsunori
authors.initials: M
authors.lastname: Shirai
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000494:pharmacology; D015703:Antigens, CD / Q000235:genetics*; D000945:Antigens, Differentiation, T-Lymphocyte / Q000235:genetics*; D018925:Chemokines / Q000276:immunology / Q000378:metabolism; D003092:Colitis / Q000139:chemically induced / Q000188:drug therapy / Q000209:etiology* / Q000401:mortality / Q000473:pathology; D003106:Colon / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D016264:Dextran Sulfate / Q000009:adverse effects; D004195:Disease Models, Animal; D037181:Lectins, C-Type / Q000037:antagonists & inhibitors / Q000172:deficiency / Q000235:genetics*; D051379:Mice; D018345:Mice, Knockout; D019707:Receptors, Chemokine / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism; D000099192:CD69 Antigens
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D018925:Chemokines; D016207:Cytokines; D016264:Dextran Sulfate; D037181:Lectins, C-Type; D019707:Receptors, Chemokine; D000099192:CD69 Antigens