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Titolo:
TUMOR-NECROSIS-FACTOR (TNF)-INDUCED CUTANEOUS NECROSIS IS MEDIATED BYTNF RECEPTOR-1
Autore:
AMAR S; VANDYKE TE; EUGSTER HP; SCHULTZE N; KOEBEL P; BLUETHMANN H;
Indirizzi:
BOSTON UNIV,SCH DENT MED,DEPT PERIODONTOL & ORAL BIOL,700 ALBANY ST BOSTON MA 02118 SWISS FED INST TECHNOL,INST TOXICOL SCHWERZENBACH SWITZERLAND F HOFFMANN LA ROCHE & CO LTD,PHARMACEUT RES GENE TECHNOL CH-4002 BASEL SWITZERLAND
Titolo Testata:
Journal of inflammation
fascicolo: 4, volume: 47, anno: 1996,
pagine: 180 - 189
SICI:
1078-7852(1996)47:4<180:T(CNIM>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
DELTA T-CELLS; KAPPA-B; ACTIVATION; ALPHA; INDUCTION; CACHECTIN; MICE; SHOCK; LIPOPOLYSACCHARIDE; INTERLEUKIN-1;
Keywords:
GENE KNOCK-OUT; TUMOR NECROSIS FACTOR; TNF RECEPTORS; SKIN NECROSIS; LIPOPOLYSACCHARIDE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
S. Amar et al., "TUMOR-NECROSIS-FACTOR (TNF)-INDUCED CUTANEOUS NECROSIS IS MEDIATED BYTNF RECEPTOR-1", Journal of inflammation, 47(4), 1996, pp. 180-189

Abstract

Tumor necrosis factor (TNF) is a central mediator of immune and inflammatory responses. Its activities have been shown to be mediated by two distinct receptors, TNFR1 (p55) and TNFR2 (p75). The cytoplasmic domains of both TNF receptors are unrelated, suggesting that they link todifferent intracellular signaling pathways. To determine their role in vivo in lipopolysaccharide (LPS)- and TNF-induced skin inflammatory necrosis, TNFR1-, TNFR2-, TNFR1/TNFR2-, and TNF lymphotoxin-alpha (LT alpha)-deficient mice were used. Skin abscesses were experimentally induced with local application of TNF or LPS. Large microscopic ulcerations were observed in TNF-injected wild-type animals and to a slightly lesser extent in TNFR2-deficient mice with tissue destruction in both cases extending deep into the dermis. Tissue destruction was accompanied by an intense immune infiltrate composed mainly of neutrophils, lymphocytes, and macrophages. TNFR1-deficient and TNFR1/TNFR2-double-deficient mice, however, did not exhibit any ulceration and showed only a very mild inflammatory infiltrate. In TNF/LT alpha-double ligand-deficient animals, a moderate epidermal necrosis was observed with a reduced inflammatory infiltrate compared to wild-type animals. As with TNF injections, subcutaneous injection of LPS induced a comparable pattern of skin necrosis in wild-type and TNF receptor mutant mice, yet a slightly more acute inflammatory level was observed regardless of the typeof animal tested. As found for TNF-induced skin necrosis, the extent of LPS-induced skin necrosis was reduced in TNF/LT alpha-deficient mice compared to wild-type animals. The present data strongly suggest that TNFR1, rather than TNFR2, is engaged in LPS- and TNF-induced skin necrosis and highlight the predominant role played by TNF in LPS-inducedinflammatory diseases. (C) 1997 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/01/21 alle ore 01:50:05