Abstract
Deficiency of the inhibitory FcgammaRIIB renders mice susceptible to autoimmune disorders characterized with cellular infiltration of target tissue. To analyze the role of FcgammaRIIB in an antibody-mediated autoimmune disease, experimental autoimmune myasthenia gravis (EAMG), FcgammaRIIB knockout (KO) and wild-type mice were immunized with acetylcholine receptor (AChR). In contrast with previous reports, FcgammaRIIB KO mice were mildly resistant to EAMG despite preserved anti-AChR antibody production and neuromuscular junction complement deposition capacity. EAMG resistance was associated with reduced lymph node cell IL-6 and IL-10 production and increased CD4(+)CD25(+) cell ratios in lymph nodes. Our data suggest that FcgammaRIIB promotes antibody-mediated autoimmunity.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antigen-Antibody Complex / blood
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Autoantibodies / immunology*
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CD4-Positive T-Lymphocytes / immunology
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Complement C3 / analysis
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Complement Membrane Attack Complex / analysis
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Cytokines / biosynthesis
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Genetic Predisposition to Disease
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Germinal Center / immunology
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Germinal Center / pathology
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Immunoglobulin G / biosynthesis
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Immunoglobulin G / immunology*
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Immunoglobulin M / biosynthesis
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Lymph Nodes / metabolism
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Lymphocyte Activation
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Myasthenia Gravis, Autoimmune, Experimental / immunology*
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Receptors, Cholinergic / immunology
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Receptors, IgG / deficiency
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Receptors, IgG / genetics
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Receptors, IgG / physiology*
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Spleen / immunology
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Spleen / pathology
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T-Lymphocyte Subsets / immunology
Substances
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Antigen-Antibody Complex
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Autoantibodies
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Complement C3
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Complement Membrane Attack Complex
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Cytokines
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Fcgr2b protein, mouse
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Immunoglobulin G
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Immunoglobulin M
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Receptors, Cholinergic
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Receptors, IgG