| Literature DB >> 14627361 |
Toyoo Nitta1, Hisashi Iwata, Yoshio Mori, Hisato Takagi, Toshio Hirota, Kazuto Kanetake, Yutaka Iida, Ken-Ichi Sakamoto, Takuya Yamada, Masanao Saio, Hajime Hirose.
Abstract
We analyzed the functional role of CD8+ T-cell receptor (TCR) Vbeta14+ T cells, which increased specifically in the lamina propria in 2,4,6-trinitrobenzene sulfonic acid (TNBS) -induced colitis. Cytotoxic activity and cytokine production in CD8+ TCR Vbeta14+ T-cell clones were analyzed by 51Cr release assay and enzyme-linked immunosorbent assay, respectively. Cell transfer studies using these clones were performed. Established T-cell clones showed specific cytotoxic activity against TNBS-conjugated self spleen cells, and this cytotoxicity was completely inhibited by anti-TCR Vbeta14 monoclonal antibody. These clones produced interferon (IFN) - gamma in their culture supernatant, but neither interleukin (IL) - 2 nor IL-4. Histological findings of the colon in mice, which received clone transfer after enema with suboptimal doses of TNBS, showed massive colitis. Our results indicate that CD8+ TCR Vbeta14+ T cells had a cytotoxic T-lymphocyte function induced by Th-1 T-cell response and played a pathogenic role in the development of TNBS-induced colitis.Entities:
Mesh:
Substances:
Year: 2003 PMID: 14627361 DOI: 10.1023/a:1026111513617
Source DB: PubMed Journal: Dig Dis Sci ISSN: 0163-2116 Impact factor: 3.199