Induction of myasthenia gravis in HLA transgenic mice by immunization with human acetylcholine receptors
H Yang, E Goluszko, C David, DK Okita… - Annals of the New …, 2003 - Wiley Online Library
H Yang, E Goluszko, C David, DK Okita, B CONTI‐FINE, TEHS CHAN, MA Poussin…
Annals of the New York Academy of Sciences, 2003•Wiley Online LibraryWe utilized HLA transgenic mice to identify the dominant epitopes on the human (H)‐AChR
α subunit. The cytoplasmic H‐AChR peptide α320–337 was the dominant T cell epitope for
DQ8, DR3, and DQ8× DQ6 F1 mice. The H‐AChR‐immunized HLA‐DQ8, DR3, DQ8× DR3
F1 and DQ8× DQ6 F1 mice developed clinical EAMG, whereas HLA‐DQ6 mice were less
susceptible.
α subunit. The cytoplasmic H‐AChR peptide α320–337 was the dominant T cell epitope for
DQ8, DR3, and DQ8× DQ6 F1 mice. The H‐AChR‐immunized HLA‐DQ8, DR3, DQ8× DR3
F1 and DQ8× DQ6 F1 mice developed clinical EAMG, whereas HLA‐DQ6 mice were less
susceptible.
Abstract: We utilized HLA transgenic mice to identify the dominant epitopes on the human (H)‐AChR α subunit. The cytoplasmic H‐AChR peptide α320–337 was the dominant T cell epitope for DQ8, DR3, and DQ8×DQ6 F1 mice. The H‐AChR‐immunized HLA‐DQ8, DR3, DQ8×DR3 F1 and DQ8×DQ6 F1 mice developed clinical EAMG, whereas HLA‐DQ6 mice were less susceptible.
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