title: Decrease of peripheral and intestinal NKG2A-positive T cells in patients with ulcerative colitis.
abstract: To investigate the role of inhibitory natural killer receptors (iNKRs) in inflammatory bowel disease (IBD), we analyzed the expression of NKG2A, one of the iNKRs, on T cells in a mouse colitis model and human IBD. During the active phase of dextran sulfate sodium (DSS)-induced mouse colitis, the frequency of NKG2A+ T cells was significantly decreased in the peripheral blood, and increased in the intestine, suggesting the mobilization of this T cell subset to the sites of inflammation. Administration of anti-NKG2A antibody increased the number of inflammatory foci in DSS-induced colitis, suggesting the involvement of NKG2A+ T cells in this colitis model. In ulcerative colitis (UC) patients, the frequency of peripheral blood NKG2A+ T cells was significantly decreased, compared with Crohn's disease (CD) patients and healthy controls, regardless of clinical conditions such as treatment modalities and disease activity. Notably, in sharp contrast to the DSS-induced mouse colitis model, the frequency of NKG2A+ cells among intestinal T cells was also decreased in UC patients. These results suggest that inadequate local infiltration of NKG2A+ T cells may be involved in the pathogenesis of UC.
authors.affiliation: Department of Pathology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
authors.forename: Takehiko
authors.initials: T
authors.lastname: Katsurada
authors.forename: Waka
authors.initials: W
authors.lastname: Kobayashi
authors.forename: Utano
authors.initials: U
authors.lastname: Tomaru
authors.forename: Tomohisa
authors.initials: T
authors.lastname: Baba
authors.forename: Shigeru
authors.initials: S
authors.lastname: Furukawa
authors.forename: Akihiro
authors.initials: A
authors.lastname: Ishizu
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Takeda
authors.forename: Naoya
authors.initials: N
authors.lastname: Sakamoto
authors.forename: Masahiro
authors.initials: M
authors.lastname: Asaka
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Takeda
authors.forename: Masanori
authors.initials: M
authors.lastname: Kasahara
mesh_terms: D000293:Adolescent; D000328:Adult; D000818:Animals; D000906:Antibodies / Q000494:pharmacology; D016022:Case-Control Studies; D002469:Cell Separation; D003093:Colitis, Ulcerative / Q000097:blood / Q000276:immunology* / Q000473:pathology*; D003424:Crohn Disease / Q000276:immunology / Q000473:pathology; D016264:Dextran Sulfate; D005260:Female; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D007413:Intestinal Mucosa / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D007422:Intestines / Q000187:drug effects / Q000276:immunology* / Q000473:pathology*; D018655:Lymphocyte Count; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008875:Middle Aged; D055654:NK Cell Lectin-Like Receptor Subfamily C / Q000276:immunology*; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology* / Q000473:pathology*; D055815:Young Adult
chemical_list: D000906:Antibodies; D055654:NK Cell Lectin-Like Receptor Subfamily C; D016264:Dextran Sulfate