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Titolo:
Cutting edge: Interactions through the IL-10 receptor regulate autoimmune diabetes
Autore:
Phillips, JM; Parish, NM; Drage, M; Cooke, A;
Indirizzi:
Univ Cambridge, Dept Pathol, Cambridge CB2 1QP, England Univ Cambridge Cambridge England CB2 1QP hol, Cambridge CB2 1QP, England
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 11, volume: 167, anno: 2001,
pagine: 6087 - 6091
SICI:
0022-1767(200112)167:11<6087:CEITTI>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
LYMPHOCYTE-ASSOCIATED ANTIGEN-4; T-CELL SUBSET; SELF-TOLERANCE; INTESTINAL INFLAMMATION; NOD MICE; DISEASE; INDUCTION; PREVENTS; INTERLEUKIN-10; MECHANISM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Cooke, A Univ Cambridge, Dept Pathol, Tennis Court Rd, Cambridge CB2 1QP, England Univ Cambridge Tennis Court Rd Cambridge England CB2 1QP England
Citazione:
J.M. Phillips et al., "Cutting edge: Interactions through the IL-10 receptor regulate autoimmune diabetes", J IMMUNOL, 167(11), 2001, pp. 6087-6091

Abstract

BDC2.5/nonobese diabetic (NOD) transgenic mice express a TCR from a diabetogenic T cell clone yet do not spontaneously develop diabetes at high incidence. Evidence exists showing that in the absence of endogenous TCR alpha-chain rearrangements this transgenic mouse spontaneously develops diabetes and that CTLA-4 negatively regulates diabetes onset. This strongly suggests that onset of diabetes in BDC2.5/NOD mice is governed by T cell regulation. We addressed the mechanism of immune regulation in BDC2.5/NOD mice. We find that activated spleen cells from young, but not old, BDC2.5/NOD mice are able to transfer diabetes to NOD-scid recipients. We have used anti-IL-10R to show that the failure of splenocytes from older mice to transfer diabetes is due to dominant regulation. We furthermore found that diabetes developed following anti-IL-10R treatment of 6-wk old BDC2.5/NOD mice indicating that endogenous IL-10 plays a key role in the regulation of diabetes onset in this transgenic mouse.

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Documento generato il 04/04/20 alle ore 15:33:47