Suppressed clinical experimental autoimmune myasthenia gravis in bm12 mice is linked to reduced intracellular calcium mobilization and IL-10 and IFN-γ release by acetylcholine receptor-specific T cells

Author:

Poussin Mathilde A,Fuller Claudette L,Goluszko Elzbieta,Reyes Victor E,Braciale Vivian L,Christadoss Premkumar

Publisher

Elsevier BV

Subject

Neurology (clinical),Neurology,Immunology,Immunology and Allergy

Reference36 articles.

1. Interferon gamma (IFN-gamma) is necessary for the genesis of acetylcholine receptor-induced clinical experimental autoimmune myasthenia gravis in mice;Balasa;J. Exp. Med.,1997

2. HLA-DQ beta-chain polymorphism linked to myasthenia gravis;Bell;Lancet,1986

3. Experimental myasthenia gravis in congenic mice. Sequence mapping and H-2 restriction of T helper epitopes on the alpha subunits of Torpedo californica and murine acetylcholine receptors;Bellone;Eur. J. Immunol.,1991

4. The I-Abm12 mutation, which confers resistance to experimental myasthenia gravis, drastically affects the epitope repertoire of murine CD4+ cells sensitized to nicotinic acetylcholine receptor;Bellone;J. Immunol.,1991

5. Distinct biochemical signals characterize agonist- and altered peptide ligand-induced differentiation of naive CD4+ T cells into Th1 and Th2 subsets;Boutin;J. Immunol.,1997

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