HLA-DQ6 transgenic mice resistance to experimental autoimmune myasthenia gravis is linked to reduced acetylcholine receptor-specific IFN-γ, IL-2 and IL-10 production
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作者:
Poussin, MA
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机构:Univ Texas, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA
Poussin, MA
Goluszko, E
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机构:Univ Texas, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA
Goluszko, E
David, CS
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机构:Univ Texas, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA
David, CS
Franco, JU
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机构:Univ Texas, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA
Franco, JU
Christadoss, P
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Univ Texas, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USAUniv Texas, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA
Christadoss, P
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机构:
[1] Univ Texas, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA
[2] Mayo Clin, Dept Immunol, Rochester, MN 55095 USA
[3] Univ Texas, Med Branch, Undergrad Summer Res Program, Galveston, TX 77550 USA
To comprehend the reduced susceptibility of HLA-DQ6 transgenic mice in comparison with HLA-DQ8 mice, to experimental autoimmune myasthenia gravis. (EAMG), we immunized them with acetylcholine receptor (AChR) and examined in vitro, the proliferative and cytokine responses to AChR. When immunized with AChR and examined for AChR-specific lymphocyte responses to AChR, EAMG-resistant DQ6 mice exhibited significantly reduced in vitro lymphoproliferative and cytokine responses to AChR, compared to DQ8 mice. The differences in susceptibility were not linked to a difference in peptide recognition by AChR-specific lymphocytes. AChR T cell epitope mapping showed that both DQ6 and DQ8 responded to the same epitopes, although to varying degrees. Resistance of DQ6 transgenic mice to EAMG was linked to a dramatic suppression of AChR-specific IFN-gamma, IL-2 and IL-10 productions by AChR-primed lymph node cells. (C) 2001 Academic Press.