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Titolo:
Relative resistance to nasally induced tolerance in non-obese diabetic mice but not other I-A(g7)-expressing mouse strains
Autore:
Quinn, A; Melo, M; Ethell, D; Sercarz, EE;
Indirizzi:
La Jolla Inst Allergy & Immunol, Div Immune Regulat, San Diego, CA 92121 USA La Jolla Inst Allergy & Immunol San Diego CA USA 92121 iego, CA 92121 USA La Jolla Inst Allergy & Immunol, Div Cellular Immunol, San Diego, CA 92121USA La Jolla Inst Allergy & Immunol San Diego CA USA 92121 Diego, CA 92121USA Univ Calif Los Angeles, Dept Microbiol & Mol Genet, Los Angeles, CA 90095 USA Univ Calif Los Angeles Los Angeles CA USA 90095 Los Angeles, CA 90095 USA
Titolo Testata:
INTERNATIONAL IMMUNOLOGY
fascicolo: 10, volume: 13, anno: 2001,
pagine: 1321 - 1333
SICI:
0953-8178(200110)13:10<1321:RRTNIT>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
MAJOR HISTOCOMPATIBILITY COMPLEX; T-CELLS; AUTOIMMUNE-DISEASES; ADOPTIVE TRANSFER; PEPTIDE-BINDING; SELF-TOLERANCE; ORAL TOLERANCE; BETA-CHAIN; SCID MICE; TH1 CELLS;
Keywords:
apoptosis; immune deviation; hen egg lysozyme; mucosal; T cells;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Quinn, A La Jolla Inst Allergy & Immunol, Div Immune Regulat, 10355 Sci Ctr Dr, SanDiego, CA 92121 USA La Jolla Inst Allergy & Immunol 10355 Sci Ctr Dr San Diego CA USA 92121
Citazione:
A. Quinn et al., "Relative resistance to nasally induced tolerance in non-obese diabetic mice but not other I-A(g7)-expressing mouse strains", INT IMMUNOL, 13(10), 2001, pp. 1321-1333

Abstract

I-A(g7) is a unique class II MHC molecule that is clearly associated with autoimmune diabetes in nonobese diabetic (NOD) mice. To determine if I-A(g7) is defective in its ability to deliver tolerogenic signals in vivo, H-2(g7) mice were nasally pretreated with antigen, prior to immunization, to induce antigen-specific regulation. Nasally pretreated NOR (H-2(g7)) and (NON). NOD (H-2(g7)) congenic mice showed responses similar to those of NON (H-2(nb1)), BALB/c (H-2(d)) and B10.PL (H-2(u)) mice a reduced recall response and a deviated Th cytokine profile. However, we found that NOD (H-2(g7)) mice are comparatively resistant to immunological tolerance induced by nasal pretreatment, such that at the usually effective dose no significant reduction was seen in the proliferative recall responses to nominal antigen after immunization. (NOD x BALB/c)F-1 (H-2(g7/d)) and (NOD x NOR)F-1 (H-2(g7)) mice were similarly resistant to nasal-induced tolerance, although significantly higher nasal doses of antigen were able to overcome the resistance in NOD and F-1 mice. Interestingly, activated NOD T cells were resistant to cell death induced by re-stimulation with plate-bound anti-CD3. These results demonstrate that activated T cells in NOD mice are defective in their ability to respond to regulatory signals delivered in vivo or in vitro. Furthermore, NOD T cells have an increased resistance to tolerance induced by I-A(g7)-dependent (antigen) or I-A(g7)-independent (anti-CD3) mechanisms. Thus, while I-Ag7 may contribute to insulin-dependent diabetes mellitus by selecting a particular repertoire of self-reactive T cell clones, additional defects in the peripheral T cells themselves are required to allow the expansion of diabetogenic clones and the development of autoimmune disease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 00:30:21