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Titolo:
MECHANISMS BY WHICH THE I-A(BM12) MUTATION INFLUENCES SUSCEPTIBILITY TO EXPERIMENTAL MYASTHENIA-GRAVIS - A STUDY IN HOMOZYGOUS AND HETEROZYGOUS MICE
Autore:
KARACHUNSKI PI; OSTLIE N; BELLONE M; INFANTE AJ; CONTIFINE BM;
Indirizzi:
UNIV MINNESOTA,COLL BIOL SCI,DEPT BIOCHEM,1479 GORTNER AVE ST PAUL MN55108 UNIV MINNESOTA,COLL BIOL SCI,DEPT BIOCHEM ST PAUL MN 55108 UNIV TEXAS,HLTH SCI CTR,DEPT PEDIAT SAN ANTONIO TX 00000 UNIV MINNESOTA,SCH MED,DEPT PHARMACOL MINNEAPOLIS MN 00000
Titolo Testata:
Scandinavian journal of immunology
fascicolo: 2, volume: 42, anno: 1995,
pagine: 215 - 225
SICI:
0300-9475(1995)42:2<215:MBWTIM>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
T-CELL RECEPTOR; V-BETA-GENE; CALIFORNICA ACETYLCHOLINE-RECEPTOR; TORPEDO-CALIFORNICA; IMMUNE RESPONSIVENESS; ALPHA-SUBUNIT; ANTIGEN; DETERMINANT; RECOGNITION; REPERTOIRE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
43
Recensione:
Indirizzi per estratti:
Citazione:
P.I. Karachunski et al., "MECHANISMS BY WHICH THE I-A(BM12) MUTATION INFLUENCES SUSCEPTIBILITY TO EXPERIMENTAL MYASTHENIA-GRAVIS - A STUDY IN HOMOZYGOUS AND HETEROZYGOUS MICE", Scandinavian journal of immunology, 42(2), 1995, pp. 215-225

Abstract

The I-A(bm12) mutation in C57B1/6 (B6) mice yields the B6.C-H-2(bm12)(bm12) strain, which is resistant to Experimental Myasthenia Gravis (EMG) induced by immunization with Torpedo acetylcholine receptor (TAChR), while the parental B6 strain is highly susceptible to EMG. CD4(+) cells from bm12 mice immunized with TAChR do not recognize three sequence regions of the TAChR alpha subunit which dominate the CD4(+) cell sensitization in B6 mice. We immunized with TAChR bm12, B6 and (bm12xB6)F1 mice. B6 and F1 mice developed EMG with comparable frequency. Their CD4(+) cells recognized the same TAChR alpha subunit peptide sequences (T alpha 150-169, T alpha 181-200 and T alpha 360-378). CD4(+) cells from TAChR-sensitized F1 mice were challenged with TAChR and alpha subunit epitope peptides, using F1, B6 or bm12 APC. B6 and F1 APC presented all these Ag efficiently, while bm12 APC presented TAChR and peptide T alpha 150-169 poorly and erratically, Anti-TAChR and anti-alphasubunit epitope CD4(+) lines propagated from F1 and B6 mice had similar TcR V beta usage. All lines but those specific for the sequence T alpha 150-169 had unrestricted V beta usage, Anti-T alpha 150-169 linesfrom both B6 and F1 mice had a strong preferential usage of V beta 6,Anti-T alpha 150-169 lines from F1 mice had also a slightly higher V beta 14 usage. B6, bm12 and F1 mice developed similar anti-TAChR Ab titres, and had Ab bound to muscle AChR in comparable amounts. ThereforeEMG resistance of bm12 mice must be due to a subtle shift in the anti-AChR Ab repertoire, and absence of special Ab able to cause destruction and/or dysfunction of muscle AChR, This is probably related to the absence of CD4(+) cells sensitized to epitopes within the sequence T alpha 150-160, consequent to the inability of the I-A(bm12) molecule topresent this sequence.

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Documento generato il 28/09/20 alle ore 15:14:17