1. Suppression of experimental autoimmune myasthenia gravis in IL-10 gene-disrupted mice is associated with reduced B cells and serum cytotoxicity on mouse cell line expressing AChR.
- Author
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Poussin MA, Goluszko E, Hughes TK, Duchicella SI, and Christadoss P
- Subjects
- Adjuvants, Immunologic genetics, Animals, Antigens, CD19 analysis, Autoantibodies blood, B-Lymphocytes chemistry, B-Lymphocytes cytology, Blood Proteins immunology, CD5 Antigens analysis, Cell Division immunology, Cell Line, Cytotoxins immunology, Epitopes immunology, Histocompatibility Antigens Class II biosynthesis, Histocompatibility Antigens Class II immunology, Immunization, Immunodominant Epitopes immunology, In Vitro Techniques, Interferon-gamma biosynthesis, Interferon-gamma immunology, Interleukin-6 biosynthesis, Interleukin-6 immunology, Lymphocyte Count, Mice, Mice, Inbred C57BL, Mice, Knockout, Muscle, Skeletal chemistry, Muscle, Skeletal immunology, Receptors, Cholinergic genetics, Tumor Necrosis Factor-alpha biosynthesis, Tumor Necrosis Factor-alpha immunology, B-Lymphocytes immunology, Interleukin-10 genetics, Interleukin-10 immunology, Myasthenia Gravis, Autoimmune, Experimental genetics, Myasthenia Gravis, Autoimmune, Experimental immunology, Receptors, Cholinergic immunology
- Abstract
To analyze the role of interleukin-10 (IL-10) in experimental autoimmune myasthenia gravis (EAMG) pathogenesis, we induced clinical EAMG in C57BL/6 and IL-10 gene-knockout (KO) mice. IL-10 KO mice had a lower incidence and severity of EAMG, with less muscle acetylcholine receptor (AChR) loss. AChR-immunized IL-10 KO mice showed a significantly higher AChR-specific proliferative response, altered cytokine response, lower number of class II-positive cells and B-cells, but a greater CD5(+)CD19(+) population than C57BL/6 mice. The lower clinical incidence in IL-10 KO could be explained not by a reduction of the quantity, but by a possible difference in the pathogenicity of anti-AChR antibodies.
- Published
- 2000
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