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Titolo:
MULTIPLICITY OF GLUCOCORTICOID ACTION IN INHIBITING ALLOGRAFT-REJECTION
Autore:
ALMAWI WY; HESS DA; RIEDER MJ;
Indirizzi:
ST GEORGE ORTHODOX HOSP,DEPT LAB MED,MOL BIOL SECT,POB 166378-6417 BEIRUT LEBANON LEBANESE NATL COUNCIL SCI RES,MED SCI UNIT BEIRUT LEBANON CHILDRENS HOSP WESTERN ONTARIO,DEPT PEDIAT LONDON ON CANADA
Titolo Testata:
Cell transplantation
fascicolo: 6, volume: 7, anno: 1998,
pagine: 511 - 523
SICI:
0963-6897(1998)7:6<511:MOGAII>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-BETA; INTERCELLULAR-ADHESION MOLECULE-1; COLONY-STIMULATING FACTOR; T-CELL ACTIVATION; BLOOD MONONUCLEAR-CELLS; TUMOR-NECROSIS-FACTOR; DEXAMETHASONE-INDUCED APOPTOSIS; INTERLEUKIN-5 GENE-EXPRESSION; RECEPTOR SIGNAL-TRANSDUCTION; LYMPHOKINE PRODUCTION INVIVO;
Keywords:
GLUCOCORTICOIDS; CYTOKINES; T CELLS; MESSENGER-RNA; TRANSPLANTATION;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
199
Recensione:
Indirizzi per estratti:
Citazione:
W.Y. Almawi et al., "MULTIPLICITY OF GLUCOCORTICOID ACTION IN INHIBITING ALLOGRAFT-REJECTION", Cell transplantation, 7(6), 1998, pp. 511-523

Abstract

Glucocorticoids (GCs) are used as immunosuppressive and antiinflammatory agents in organ transplantation and in treating autoimmune diseases and inflammatory disorders. GCs were shown to exert their antiproliferative effects directly through blockade of certain elements of an early membrane-associated signal transduction pathway, modulation of theexpression of select adhesion molecules, and by suppression of cytokine synthesis and action. GCs may act indirectly by inducing lipocortinsynthesis, which in turn, inhibits arachidonic acid release from membrane-bound stores, and also by inducing transforming growth factor (TGF)-beta expression that subsequently blocks cytokine synthesis and T cell activation. Furthermore, by preferentially inhibiting the production of Th1 cytokines, GCs may enhance Th2 cell activity and, hence, precipitate a long-lasting state of tolerance through a preferential promotion of a Th2 cytokine-secreting profile. In exerting their antiproliferative effects, GCs influence both transcriptional and posttranscriptional events by binding their cytosolic receptor (GR), which subsequently binds the promoter region of cytokine genes on select DNA sites compatible with the GCs responsible elements (GRE) motif. In addition to direct DNA binding, GCs may also directly bind to, and hence antagonize, nuclear factors required for efficient gene expression, thereby markedly reducing transcriptional rate. The pleiotrophy of the GCs action, coupled with the diverse experimental conditions employed in assessing the GCs effects, indicate that GCs may utilize more than one mechanism in inhibiting T cell activation, and warrant careful scrutiny inassigning a mechanism by which GCs exert their antiproliferative effects. (C) 1998 Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/07/20 alle ore 18:11:45