Immunoglobulin G–mediated Inflammatory Responses Develop Normally in Complement-deficient Mice
| Autor: | Michael C. Carroll, Diana Sylvestre, Minga Ma, Raphael Clynes, Jeffrey V. Ravetch, Henry B. Warren |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Blood Platelets
Anemia Hemolytic Erythrocytes Neutrophils Immunology Inflammation Biology Article Immunoglobulin G Immune Hemolytic Anemia Mice 03 medical and health sciences 0302 clinical medicine Immune system Phagocytosis medicine Animals Immunology and Allergy Cytotoxic T cell Receptor 030304 developmental biology Mice Knockout 0303 health sciences Arthus reaction Complement C4 Complement C3 Articles medicine.disease Thrombocytopenia 3. Good health biology.protein Rabbits medicine.symptom Antibody 030215 immunology |
| Zdroj: | The Journal of Experimental Medicine |
| ISSN: | 1540-9538 0022-1007 |
| Popis: | The role of complement in immunoglobulin G–triggered inflammation was studied in mice genetically deficient in complement components C3 and C4. Using the reverse passive Arthus reaction and experimental models of immune hemolytic anemia and immune thrombocytopenia, we show that these mice have types II and III inflammatory responses that are indistinguishable from those of wild-type animals. Complement-deficient and wild-type animals exhibit comparable levels of erythrophagocytosis and platelet clearance in response to cytotoxic anti–red blood cell and antiplatelet antibodies. Furthermore, in the reverse passive Arthus reaction, soluble immune complexes induce equivalent levels of hemmorhage, edema, and neutrophillic infiltration in complement-deficient and wild-type animals. In contrast, mice that are genetically deficient in the expression of Fc receptors exhibit grossly diminished reactions by both cytotoxic antibodies and soluble immune complexes. These studies provide strong evidence that the activation of cell-based FcγR receptors, but not complement, are required for antibody-triggered murine inflammatory responses. |
| Databáze: | OpenAIRE |
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