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Titolo:
IL-12 plays a pivotal role in LFA-1-mediated T cell adhesiveness by up-regulation of CCR5 expression
Autore:
Mukai, T; Iwasaki, M; Gao, P; Tomura, M; Yashiro-Ohtani, Y; Ono, S; Murai, M; Matsushima, K; Kurimoto, M; Kogo, M; Matsuya, T; Fujiwara, H; Hamaoka, T;
Indirizzi:
Osaka Univ, Grad Sch Med, Biomed Res Ctr, Dept Oncol, Suita, Osaka 5650871, Japan Osaka Univ Suita Osaka Japan 5650871 t Oncol, Suita, Osaka 5650871, Japan Osaka Univ, Grad Sch Dent, Div Pathogenesis & Control Oral Dis, Osaka, Japan Osaka Univ Osaka Japan iv Pathogenesis & Control Oral Dis, Osaka, Japan Univ Tokyo, Fac Med, Dept Mol Prevent Med, Tokyo, Japan Univ Tokyo TokyoJapan kyo, Fac Med, Dept Mol Prevent Med, Tokyo, Japan Fujisaki Inst, Hayashibara Biochem Labs, Okayama, Japan Fujisaki Inst Okayama Japan t, Hayashibara Biochem Labs, Okayama, Japan
Titolo Testata:
JOURNAL OF LEUKOCYTE BIOLOGY
fascicolo: 3, volume: 70, anno: 2001,
pagine: 422 - 430
SICI:
0741-5400(200109)70:3<422:IPAPRI>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHEMOKINE RECEPTORS; CHEMOTACTIC RESPONSIVENESS; GAMMA RECEPTOR; HOST-DEFENSE; MICE LACKING; IFN-GAMMA; LYMPHOCYTES; CLONING; RECRUITMENT; CDNA;
Keywords:
chemokine; chemokine receptor; adhesion molecule;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Fujiwara, H Osaka Univ, Grad Sch Med, Biomed Res Ctr, Dept Oncol, 2-2 Yamadaoka, Suita, Osaka 5650871, Japan Osaka Univ 2-2 Yamadaoka Suita Osaka Japan 5650871 0871, Japan
Citazione:
T. Mukai et al., "IL-12 plays a pivotal role in LFA-1-mediated T cell adhesiveness by up-regulation of CCR5 expression", J LEUK BIOL, 70(3), 2001, pp. 422-430

Abstract

The chemokine receptor CCR5 has been implicated in the recruitment of T cells to inflammatory sites. However, the regulation of CCR5 induction on T cells and its contribution to T cell adhesiveness are poorly understood. Using a Th1 clone, 2D6, that can be maintained with interleukin (IL)-12 or IL-2 alone (designated 2D6(IL-12) or 2D6(IL-2), respectively), we investigatedhow CCR5 is induced on T cells and whether CCR5 is responsible for up-regulating the function of adhesion molecules. 2D6(IL-12) grew, forming cell aggregates, in culture containing IL-12. This was due to lymphocyte function-associated antigen (LFA)-1-intercellular adhesion molecule (ICAM)-1 interaction, because 2D6(IL-12) expressed both LFA-1 and ICAM-1 and cell aggregation was inhibited by anti-ICAM-1 monoclonal antibody. Despite comparable levels of LFA-1 and ICAM-1 expression, 2D6(IL-2) cells did not aggregate in culture with IL-2. It is important that there was a critical difference in CCR5 expression between 2D6 IL-12 and 2D6(IL-2); the former expressed high levels of CCR5, and the latter expressed only marginal levels. Both types of cells expressed detectable albeit low levels of RANTES (regulated on activation, normal T expressed and secreted) mRNA. Unlike IL-12 or IL-2, IL-18 induced high levels of RANTES mRNA expression without modulating CCR5 expression. Therefore, combined stimulation with IL-12 and IL-18 strikingly up-regulated 2D6 cell aggregation. Notably, LFA-1-mediated aggregation of 2D6(IL-12) cells was suppressed by anti-CCR5 antibody. These results indicate thatIL-12 plays a critical role in CCR5 expression on Th1 cells and consequently contributes to CCR5-mediated activation of LFA-1 molecules.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 08:34:28