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Titolo:
AN ACETYLCHOLINE-RECEPTOR ALPHA-SUBUNIT PROMOTER CONFERS INTRATHYMIC EXPRESSION IN TRANSGENIC MICE - IMPLICATIONS FOR TOLERANCE OF A TRANSGENIC SELF-ANTIGEN AND FOR AUTOREACTIVITY IN MYASTHENIA-GRAVIS
Autore:
SALMON AM; BRUAND C; CARDONA A; CHANGEUX JP; BERRIHAKNIN S;
Indirizzi:
HOP MARIE LANNELONGUE,CNRS,UPRESA,IMMUNOL LAB,133 AVE RESISTANCE F-92350 LE PLESSIS ROBINS FRANCE HOP MARIE LANNELONGUE,CNRS,UPRESA,IMMUNOL LAB F-92350 LE PLESSIS ROBINS FRANCE HOP MARIE LANNELONGUE,CNRS,UPRESA,LAB PHYSIOL THYM,IPSC F-92350 LE PLESSIS ROBINS FRANCE INST PASTEUR,CNRS URA 1284,UNITE NEUROBIOL MOL F-75015 PARIS FRANCE INST PASTEUR,LAB TECHNOL CELLULAIRE F-75724 PARIS 15 FRANCE
Titolo Testata:
The Journal of clinical investigation
fascicolo: 11, volume: 101, anno: 1998,
pagine: 2340 - 2350
SICI:
0021-9738(1998)101:11<2340:AAAPCI>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
T-CELL TOLERANCE; CLONAL DELETION; B-CELLS; THYMIC EPITHELIUM; CD4+8+ THYMOCYTES; INDUCTION; THYMOMAS; ANTIBODIES; PROTEIN; MUSCLE;
Keywords:
THYMUS; MYOID CELLS; EPITHELIAL CELLS; TH1/TH2; ANTIBODY RESPONSE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
56
Recensione:
Indirizzi per estratti:
Citazione:
A.M. Salmon et al., "AN ACETYLCHOLINE-RECEPTOR ALPHA-SUBUNIT PROMOTER CONFERS INTRATHYMIC EXPRESSION IN TRANSGENIC MICE - IMPLICATIONS FOR TOLERANCE OF A TRANSGENIC SELF-ANTIGEN AND FOR AUTOREACTIVITY IN MYASTHENIA-GRAVIS", The Journal of clinical investigation, 101(11), 1998, pp. 2340-2350

Abstract

Myasthenia gravis (MG) is an autoimmune disease targeting the skeletal muscle acetylcholine receptor (AChR). Although the autoantigen is present in the thymus, it is not tolerated in MG patients. In addition, the nature of the cell bearing the autoantigen is controversial. To approach these questions, we used two lineages of transgenic mice in which the beta-galactosidase (beta-gal) gene is under the control of a 842-bp (Tg1) or a 3300-bp promoter fragment (Tg2) of the chick muscle cwsubunit AChR gene. In addition to expression in muscle cells, thymic expression was observed in both mouse lines (mainly in myoid cells in Tg1 and myoid cells and epithelial cells in Tg2). After challenge withbeta-gar, Tg1 mice produced Th2-dependent anti-beta-gal antibodies, while Tg2 mice were almost unresponsive. By contrast, in a proliferation assay both Tg lines were unresponsive to beta-gal. Cells from Tg1 mice produce Th2-dependent cytokine whereas cells from Tg2 mice were nonproducing in response to beta-gal. These data indicate that the level of expression in Tg1 mice could be sufficient to induce tolerance of Th1 cells but not of Th2 cells, while both populations are tolerated inTg2 mice. These findings are compatible with the hypothesis that AChRexpression is not sufficiently abundant in MG thymus to induce a fulltolerance.

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Documento generato il 30/11/20 alle ore 19:59:04