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Titolo:
Nonlymphocyte-derived tumor necrosis factor is required for induction of colitis in recombination activating gene (RAG)2(-/-) mice upon transfer of CD4(+)CD45RB(hi) T cells
Autore:
Corazza, N; Eichenberger, S; Eugster, HP; Mueller, C;
Indirizzi:
Univ Bern, Inst Pathol, Div Immunopathol, CH-3010 Bern, Switzerland Univ Bern Bern Switzerland CH-3010 munopathol, CH-3010 Bern, Switzerland Univ Zurich Hosp, Dept Internal Med, CH-8057 Zurich, Switzerland Univ Zurich Hosp Zurich Switzerland CH-8057 CH-8057 Zurich, Switzerland
Titolo Testata:
JOURNAL OF EXPERIMENTAL MEDICINE
fascicolo: 10, volume: 190, anno: 1999,
pagine: 1479 - 1491
SICI:
0022-1007(19991115)190:10<1479:NTNFIR>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
INFLAMMATORY BOWEL-DISEASE; CROHNS-DISEASE; DEFICIENT MICE; FACTOR-ALPHA; TNF-ALPHA; SCID MICE; INTERLEUKIN-10-DEFICIENT MICE; PROINFLAMMATORY CYTOKINES; ULCERATIVE-COLITIS; LYMPHOTOXIN-ALPHA;
Keywords:
inflammatory bowel disease; mucosal immunity; intestinal inflammation; proinflammatory cytokines;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Mueller, C Univ Bern, Inst Pathol, Div Immunopathol, Murtenstr 31, CH-3010Bern, Switzerland Univ Bern Murtenstr 31 Bern Switzerland CH-3010 n, Switzerland
Citazione:
N. Corazza et al., "Nonlymphocyte-derived tumor necrosis factor is required for induction of colitis in recombination activating gene (RAG)2(-/-) mice upon transfer of CD4(+)CD45RB(hi) T cells", J EXP MED, 190(10), 1999, pp. 1479-1491

Abstract

In this study, we addressed the role of tumor necrosis factor (TNF)-alpha and lymphotoxin (LT)-alpha in the development of colitis and defined the cellular sources (T cells versus non-T cells) of TNF (TNF-alpha and LT-alpha)relevant to disease development. After adoptive transfer of TNF+/+ CD4(+)CD45RB(hi) splenocytes into TNF+/+ recombination activating gene (RAG)2(-/-)mice, the recipients develop massive inflammation of the large intestinal mucosa concurrent with massive weight loss. In contrast, clinical signs of disease are completely absent in TNF(-/-)RAG2(-/-) recipients of TNF-/- CD4(+)CD45RB(hi) T cells, although elevated numbers of interferon-gamma-producing cells are present in die colonic mucosa. Surprisingly, upon transfer ofTNF(-/-)CD4(+)CD45RB(hi) T cells into TNF(+/+)RAG2(-/-) recipients, colitis develops with kinetics similar to those upon transfer of TNF(+/+)CD4(+)CD45RB(hi) donor cells. In contrast, no clinical signs of colitis are observed ill TNF(-/-)RAG2(-/-) recipients of TNF(+/+)CD4(+)CD45RB(hi) T cells. This protection from colitis is not a consequence of the absence of LT-alpha. as TNF-alpha(-/-)RAG2(-/-) recipients of TNF-alpha(-/-) CD4(+)CD45RB(hi) T cells are also protected from colitis induction. These results demonstrate the importance of TNF production by non-T cells of die colonic mucosa in the pathogenesis of colitis and provide direct evidence for a nonredundant role of TNF-alpha ill this mouse model of colitis.

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Documento generato il 27/01/21 alle ore 02:39:45