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Titolo:
Regulation of CD40 ligand expression in systemic lupus erythematosus
Autore:
Crow, MK; Kirou, KA;
Indirizzi:
Cornell Univ, Hosp Special Surg, Dept Med, New York, NY 10021 USA Cornell Univ New York NY USA 10021 Surg, Dept Med, New York, NY 10021 USA Cornell Univ, Weill Med Coll, New York, NY USA Cornell Univ New York NY USA nell Univ, Weill Med Coll, New York, NY USA
Titolo Testata:
CURRENT OPINION IN RHEUMATOLOGY
fascicolo: 5, volume: 13, anno: 2001,
pagine: 361 - 369
SICI:
1040-8711(200109)13:5<361:ROCLEI>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
T-CELL ACTIVATION; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MESSENGER-RNA STABILIZATION; HUMAN ENDOTHELIAL-CELLS; NECROSIS-FACTOR-ALPHA; B-CELLS; RHEUMATOID-ARTHRITIS; MULTIPLE-SCLEROSIS; SOLUBLE CD40; DEPENDENT ACTIVATION;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
102
Recensione:
Indirizzi per estratti:
Indirizzo: Crow, MK Cornell Univ, Hosp Special Surg, Dept Med, 535 E 70th St, New York, NY 10021 USA Cornell Univ 535 E 70th St New York NY USA 10021 rk, NY 10021 USA
Citazione:
M.K. Crow e K.A. Kirou, "Regulation of CD40 ligand expression in systemic lupus erythematosus", CURR OP RH, 13(5), 2001, pp. 361-369

Abstract

Production of pathogenic autoantibodies in systemic lupus erythematosus (SLE) requires T cell help, along with ligation of the B cell surface immunoglobulin receptor by antigen. It is likely that macrophages, dendritic cells, and endothelial cells are also activated by interactions with T cells andcontribute to lupus pathology. CD40 ligand (CD40L, CD154), a member-of thetumor necrosis factor family of cell surface molecules, mediates these contact dependent signals delivered by CD4(+) T helper cells to CD40(+) targetcells. Recent data from SLE patients and murine lupus models have demonstrated prolonged expression of CD40L on lupus T cells and its capacity to mediate excessive B cell activation. This review summarizes the current information regarding transcriptional and post-transcriptional regulation of CD40L expression in normal and SLE T cells. More complete characterization of the mechanisms that regulate the magnitude and duration of CD40L expression should suggest new approaches to modulate this promising therapeutic target. (C) 2001 Lippincott Williams & Wilkins, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 03:36:36