Abstract
C5 deficient mice are highly resistant to experimental autoimmune myasthenia gravis (EAMG) despite intact immune response to acetylcholine receptor (AChR), validating the pivotal role played by membrane attack complex (MAC, C5b-9) in neuromuscular junction destruction. To distinguish the significance of C5a from that of C5b in EAMG pathogenesis, C5a receptor (C5aR) knockout (KO) and wild-type (WT) mice were immunized with AChR to induce pathogenic anti-AChR antibodies. In contrast with C5 deficient mice, C5aR KO mice were equally susceptible to EAMG as WT mice and exhibited comparable antibody and lymphocyte proliferation response to AChR implicating that C5a is not involved in EAMG development.
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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Antibodies / metabolism
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Antigen-Antibody Complex
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Complement C5a / genetics
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Complement C5a / metabolism
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Disease Models, Animal
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Enzyme-Linked Immunosorbent Assay / methods
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Germinal Center / immunology
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Mice
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Mice, Knockout
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Myasthenia Gravis, Autoimmune, Experimental / genetics
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Myasthenia Gravis, Autoimmune, Experimental / immunology*
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Radioimmunoassay / methods
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Receptor, Anaphylatoxin C5a / deficiency
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Receptor, Anaphylatoxin C5a / physiology*
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Receptors, Cholinergic / immunology*
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Statistics, Nonparametric
Substances
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Antibodies
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Antigen-Antibody Complex
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Receptor, Anaphylatoxin C5a
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Receptors, Cholinergic
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Complement C5a