Specific CTL activity of CD8+ TCR Vbeta14+ T cell in mouse 2, 4, 6-trinitrobenzene sulfonic acid-induced colitis.
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.
Nitta
Toyoo
T
First Department of Surgery, Gifu University School of Medicine, 40 Tsukasamachi, Gifu City, Gifu 5008705, Japan. toyoo@par.odn.ne.jp
Iwata
Hisashi
H
Mori
Yoshio
Y
Takagi
Hisato
H
Hirota
Toshio
T
Kanetake
Kazuto
K
Iida
Yutaka
Y
Sakamoto
Ken-Ichi
K
Yamada
Takuya
T
Saio
Masanao
M
Hirose
Hajime
H
D019264:Adoptive Transfer; D000818:Animals; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism*; D002999:Clone Cells; D003092:Colitis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000378:metabolism*; D013602:T-Lymphocytes, Cytotoxic; D014302:Trinitrobenzenesulfonic Acid
D016693:Receptors, Antigen, T-Cell, alpha-beta; D014302:Trinitrobenzenesulfonic Acid