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Abstract
Complement activation is one of the most powerful mechanisms taking place during inflammation and immune responses. Over the last 30 years increasing evidence has proven the role of C3 and receptors for its activation fragments in the initiation and regulation of immune responses. Since complement also has a basic importance in the maintenance of immune homeostasis, abnormalities affecting complement proteins and their receptors may lead to pathological conditions. Autoimmune conditions develop as a result of a range of genetic and environmental factors. Findings obtained from animal models support the notion that malfunctioning of complement receptors, particularly CR2, might be involved in the breakdown of tolerance and excessive antibody production by auto reactive B-cell clones. In addition to B cells, activated, CR2-bearing T cells may also contribute to the pathogenesis of autoimmunity as they can receive activating/survival signals in the inflamed tissue. Results obtained from mouse experiments however, should be extended to the human system with great care, since there are basic differences between the structure and function of human and murine CR1 and CR2.
| Abbreviations | ||
| APC | = | antigen presenting cell |
| BCR | = | B cell receptor |
| CIA | = | collagen induced arthritis |
| CR | = | complement receptor |
| FDC | = | follicular dendritic cell |
| GC | = | germinal center |
| MZ | = | marginal zone |
| mAb | = | monoclonal antibody |
| RA | = | rheumatoid arthritis |
| SCR | = | short consensus repeat |
| SLE | = | systemic lupus erythematosus |
| sCR2 | = | soluble CR2 |
| Abbreviations | ||
| APC | = | antigen presenting cell |
| BCR | = | B cell receptor |
| CIA | = | collagen induced arthritis |
| CR | = | complement receptor |
| FDC | = | follicular dendritic cell |
| GC | = | germinal center |
| MZ | = | marginal zone |
| mAb | = | monoclonal antibody |
| RA | = | rheumatoid arthritis |
| SCR | = | short consensus repeat |
| SLE | = | systemic lupus erythematosus |
| sCR2 | = | soluble CR2 |
Acknowledgements
The financial support of Hungarian National Science Fund (OTKA) TS044711, T047151 and that of NKFP 1A/040/04 are gratefully acknowledged.