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Titolo:
Lymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis
Autore:
Goluszko, E; Hjelmstrom, P; Deng, CS; Poussin, MA; Ruddle, NH; Christadoss, P;
Indirizzi:
Univ Texas, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 biol & Immunol, Galveston, TX 77555 USA Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06520 USA Yale Univ New Haven CT USA 06520 iol & Publ Hlth, New Haven, CT 06520 USA Yale Univ, Sch Med, Immunobiol Sect, New Haven, CT 06520 USA Yale Univ New Haven CT USA 06520 Immunobiol Sect, New Haven, CT 06520 USA Karolinska Inst, Dept Med, S-17176 Stockholm, Sweden Karolinska Inst Stockholm Sweden S-17176 Med, S-17176 Stockholm, Sweden
Titolo Testata:
JOURNAL OF NEUROIMMUNOLOGY
fascicolo: 1, volume: 113, anno: 2001,
pagine: 109 - 118
SICI:
0165-5728(20010201)113:1<109:LDCPCM>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACETYLCHOLINE-RECEPTOR; IFN-GAMMA; THYMUS; POLYMORPHISMS; GENES; MATURATION; INDUCTION; THERAPY; DISEASE;
Keywords:
autoimmunity; myasthenia gravis; acetylcholine receptors; cytokines; lymphotoxins; TNF receptors;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Christadoss, P Univ Texas, Med Branch, Dept Microbiol & Immunol, 301 Univ Blvd,3-142 MRB,Galveston, TX 77555 USA Univ Texas 301 Univ Blvd,3-142 MRB Galveston TX USA 77555 A
Citazione:
E. Goluszko et al., "Lymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis", J NEUROIMM, 113(1), 2001, pp. 109-118

Abstract

A complete prevention of clinical experimental autoimmune myasthenia gravis (EAMG) was observed in lymphotoxin (LT)-alpha deficient (LT-alpha (-/-)) mice compared to LT-alpha (+/+) mice when immunized with acetylcholine receptor. However, only a partial prevention of clinical EAMG incidence was observed in LT-beta (-/-) mice compared to LT-beta (-/-) mice. LT-alpha (-/-) and LT-beta (-/-) mice had lower mean titers of total IgG, IgG(1), IgG(2a) and IgG(2b) and higher or equal mean titers of IgM anti AChR antibodies compared to controls. Therefore. LT-alpha (-/-) and LT-beta (-/-) AChR immunized mice are capable of mounting a primary (IgM) humoral immune response to AChR, but are less capable of switching to the pathogenic anti-AChR IgG isotypes. LT could play a significant role in the pathogenesis of myasthenia gravis. (C) 2001 Elsevier Science B.V. All rights reserved.

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Documento generato il 22/09/20 alle ore 23:36:46