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Titolo:
Cutting edge: NKG2D receptors induced by IL-15 costimulate CD28-negative effector CTL in the tissue microenvironment
Autore:
Roberts, AI; Lee, L; Schwarz, E; Groh, V; Spies, T; Ebert, EC; Jabri, B;
Indirizzi:
Univ Med & Dent New Jersey, Dept Med, New Brunswick, NJ 08903 USA Univ Med& Dent New Jersey New Brunswick NJ USA 08903 swick, NJ 08903 USA Princeton Univ, Dept Mol Biol, Princeton, NJ 08544 USA Princeton Univ Princeton NJ USA 08544 t Mol Biol, Princeton, NJ 08544 USA Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98109 USA Fred Hutchinson Canc Res Ctr Seattle WA USA 98109 , Seattle, WA 98109 USA
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 10, volume: 167, anno: 2001,
pagine: 5527 - 5530
SICI:
0022-1767(20011115)167:10<5527:CENRIB>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
CYTOLYTIC T-LYMPHOCYTES; INTRAEPITHELIAL LYMPHOCYTES; INHIBITORY RECEPTORS; DENDRITIC CELLS; NK RECEPTORS; IN-VIVO; ACTIVATION; EXPRESSION; INTERLEUKIN-15; CYTOTOXICITY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Jabri, B Princeton Univ, Schultz Lab, Dept Mol Biol, Washington Rd, Princeton, NJ 08540 USA Princeton Univ Washington Rd Princeton NJ USA 08540 NJ 08540 USA
Citazione:
A.I. Roberts et al., "Cutting edge: NKG2D receptors induced by IL-15 costimulate CD28-negative effector CTL in the tissue microenvironment", J IMMUNOL, 167(10), 2001, pp. 5527-5530

Abstract

Unlike primary T cells in lymph nodes, effector CD8(+) CTL in tissues do not express the costimulatory receptor CD28. We report that NKG2D, the receptor for stress-induced MICA and MICB molecules expressed in the intestine, serves as a potent costimulatory receptor for CTL freshly isolated from thehuman intestinal epithelium. Expression and function of NKG2D are selectively up-regulated by the cytokine IL-15, which is released by the inflamed intestinal epithelium. These findings identify a novel CTL costimulatory pathway regulated by IL-15 and suggest that tissues can fine-tune the activation of effector T cells based on the presence or absence of stress and inflammation. Uncontrolled secretion of IL-15 could lead to excessive induction of NKG2D and thus contribute to the development of autoimmune disease by facilitating the activation of autoreactive T cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 00:45:00