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Faust, KB; Finke, D; Klempt-Giessing, K; Randers, K; Zachrau, B; Schlenke, P; Kirchner, H; Goerg, S.
Antigen-induced B cell apoptosis is independent of complement C4.
Clin Exp Immunol. 2007; 150(1): 132-139. Doi: 10.1111/j.1365-2249.2007.03456.x [OPEN ACCESS]
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Co-authors Med Uni Graz
Schlenke Peter
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Abstract:
Deficiencies in early complement components are associated with the development of systemic lupus erythematosus (SLE) and therefore early complement components have been proposed to influence B lymphocyte activation and tolerance induction. A defect in apoptosis is a potential mechanism for breaking of peripheral B cell tolerance, and we hypothesized that the lack of the early complement component C4 could initiate autoimmunity through a defect in peripheral B lymphocyte apoptosis. Previous studies have shown that injection of a high dose of soluble antigen, during an established primary immune response, induces massive apoptotic death in germinal centre B cells. Here, we tested if the antigen-induced apoptosis within germinal centres is influenced by early complement components by comparing complement C4-deficient mice with C57BL/6 wild-type mice. We demonstrate that after the application of a high dose of soluble antigen in wild-type mice, antibody levels declined temporarily but were restored almost completely after a week. However, after antigen-induced apoptosis, B cell memory was severely limited. Interestingly, no difference was observed between wild-type and complement C4-deficient animals in the number of apoptotic cells, restoration of antibody levels and memory response.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Antigens - immunology
Apoptosis - immunology
B-Lymphocytes - immunology
Complement C4 - deficiency Complement C4 - immunology
Enzyme-Linked Immunosorbent Assay - methods
Female -
Germinal Center - immunology
Immune Tolerance -
Immunologic Memory -
Lupus Erythematosus, Systemic - immunology
Mice -
Mice, Inbred C57BL -
Nitrophenols - immunology
Phenylacetates -

Find related publications in this database (Keywords)
apoptosis
complement
memory
SLE
tolerance
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