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Titolo:
Prodigiosin blocks T cell activation by inhibiting interleukin-2R alpha expression and delays progression of autoimmune diabetes and collagen-inducedarthritis
Autore:
Han, SB; Park, SH; Jeon, YJ; Kim, YK; Kim, HM; Yang, KH;
Indirizzi:
Korea Adv Inst Sci & Technol, Dept Biol Sci, Taejon 305701, South Korea Korea Adv Inst Sci & Technol Taejon South Korea 305701 5701, South Korea Korea Res Inst Biosci & Biotechnol, Taejon, South Korea Korea Res Inst Biosci & Biotechnol Taejon South Korea ejon, South Korea
Titolo Testata:
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
fascicolo: 2, volume: 299, anno: 2001,
pagine: 415 - 425
SICI:
0022-3565(200111)299:2<415:PBTCAB>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
RECEPTOR-ALPHA GENE; NF-KAPPA-B; PHOSPHATIDYLINOSITOL 3-KINASE; MOLECULAR TARGETS; PROTEIN-KINASE; NOD MICE; IL-2; PROLIFERATION; TRANSCRIPTION; IMMUNOSUPPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Kim, HM Korea Res Inst Biosci & Biotechnol, POB 115, Yusong 305600, Daejon, South Korea Korea Res Inst Biosci & Biotechnol POB 115 Yusong Daejon South Korea 305600
Citazione:
S.B. Han et al., "Prodigiosin blocks T cell activation by inhibiting interleukin-2R alpha expression and delays progression of autoimmune diabetes and collagen-inducedarthritis", J PHARM EXP, 299(2), 2001, pp. 415-425

Abstract

Prodigiosin (PDG) was previously reported to be a T cell-specific immunosuppressant. Here we describe the mechanism of action of PDG in T cells and the effect of PDG on autoimmune diseases. PDG selectively suppresses concanavalin A (Con A)-induced T cell proliferation, but has little effect on lipopolysaccharide-induced proliferation of B cells and nitric oxide productionof macrophages. Although PDG does not block interleukin (IL)-2 production,it efficiently inhibits interleukin-2 receptor alpha -chain (IL-2R alpha) expression, and this results in a disruption of the IL-2/IL-2R signaling pathway, on which a great part of the regulation of T cell activation depends. PDG blocks T cell differentiation into effector helper T cells secreting interferon-gamma and IL-4 as well as into effector cytotoxic T lymphocytes expressing perforin, which is at least in part resulting from inhibition ofthe IL-2/IL-2R signaling. PDG indirectly blocks signal transducer and activator of transcription activation by inhibiting cytokine signalings in Con A-activated T cells, although it does not inhibit the activation of nuclearfactor-kappaB, nuclear factor of activated T cells, and activator protein-1. As direct evidence of immunosuppression in vivo, we show that PDG markedly reduced blood glucose levels and cellular infiltration into the pancreatic islets in nonobese diabetic mice, and that it also delays the onset of collagen-induced arthritis in DBA/1 mice. In conclusion, our results demonstrate that PDG has a unique mode of action, namely, that it blocks T cell activation by inhibiting primarily IL-2R alpha expression in the IL-2/ IL-2R signaling, and show that this compound represents a promising immunosuppressant candidate for the treatment of autoimmune diseases.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 19:34:12