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Titolo:
Blockade of interleukin 6 trans signaling suppresses T-cell resistance against apoptosis in chronic intestinal inflammation: Evidence in Crohn disease and experimental colitis in vivo
Autore:
Atreya, R; Mudter, J; Finotto, S; Mullberg, J; Jostock, T; Wirtz, S; Schutz, M; Bartsch, B; Holtmann, M; Becker, C; Strand, D; Czaja, J; Schlaak, JF; Lehr, HA; Autschbach, F; Schurmann, G; Nishimoto, N; Yoshizaki, K; Ito, H; Kishimoto, T; Galle, PR; Rose-John, S; Neurath, MF;
Indirizzi:
Univ Mainz, Med Clin 1, Immunol Lab, D-55131 Mainz, Germany Univ Mainz Mainz Germany D-55131 1, Immunol Lab, D-55131 Mainz, Germany Univ Mainz, Med Clin 1, Sect Pathophysiol, D-55131 Mainz, Germany Univ Mainz Mainz Germany D-55131 ct Pathophysiol, D-55131 Mainz, Germany Univ Mainz, Inst Pathol, D-55131 Mainz, Germany Univ Mainz Mainz GermanyD-55131 nz, Inst Pathol, D-55131 Mainz, Germany Univ Heidelberg, Inst Pathol, D-69120 Heidelberg, Germany Univ HeidelbergHeidelberg Germany D-69120 , D-69120 Heidelberg, Germany Univ Munster, Dept Surg, D-48129 Munster, Germany Univ Munster Munster Germany D-48129 Dept Surg, D-48129 Munster, Germany
Titolo Testata:
NATURE MEDICINE
fascicolo: 5, volume: 6, anno: 2000,
pagine: 583 - 588
SICI:
1078-8956(200005)6:5<583:BOI6TS>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
NECROSIS-FACTOR-ALPHA; BOWEL-DISEASE; IL-6 RECEPTOR; MICE; STAT3; ACTIVATION; TERM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Neurath, MF Univ Mainz, Med Clin 1, Immunol Lab, D-55131 Mainz, Germany Univ Mainz Mainz Germany D-55131 Lab, D-55131 Mainz, Germany
Citazione:
R. Atreya et al., "Blockade of interleukin 6 trans signaling suppresses T-cell resistance against apoptosis in chronic intestinal inflammation: Evidence in Crohn disease and experimental colitis in vivo", NAT MED, 6(5), 2000, pp. 583-588

Abstract

The pro-inflammatory cytokine interleukin (IL)-6 (refs. 1-5) can bind to cells lacking the IL-6 receptor (IL-6R) when it forms a complex with the soluble IL-6R (sIL-6R) (trans signaling)(5-7). Here, we have assessed the contribution of this system to the increased resistance of mucosal T cells against apoptosis in Crohn disease (CD), a chronic inflammatory disease of the gastrointestinal tract(8-12). A neutralizing antibody against IL-6R suppressed established experimental colitis in various animal models of CD mediated by type 1 T-helper cells, by inducing apoptosis of lamina propria T cells. Similarly, specific neutralization of sIL-6R in vivo by a newly designed gp130-Fc fusion protein caused suppression of colitis activity and induction of apoptosis, indicating that sIL-6R prevents mucosal T-cell apoptosis. In patients with Co, mucosal T cells showed strong evidence for IL-6 trans signaling, with activation of signal transducer and activator of transcription 3, bcl-2 and bcl-xl. Blockade of IL-6 trans signaling caused T-cell apoptosis, indicating that the IL-6-sIL-6R system mediates the resistance of T cells to apoptosis in CD. These data indicate that a pathway of T-cell activation driven by IL-6-sIL-6R contributes to the perpetuation of chronic intestinal inflammation. Specific targeting of this pathway may be a promisingnew approach for the treatment of CD.

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Documento generato il 09/07/20 alle ore 01:37:26