Lack of high avidity IgM anti-ssDNA antibodies in cells from autoimmune-prone and autoimmune mice |
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Authors: | A Panoskaltsis N R Sinclair |
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Affiliation: | Department of Microbiology and Immunology, University of Western Ontario, London, Canada. |
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Abstract: | Non-autoimmune prone CBA mice were compared with autoimmune prone NZB, NZW, and (NZB x NZW)F1 mice for the ability of their splenic cells to produce anti-ssDNA-forming cells spontaneously in vitro, measured in the plaque forming cell assay. The number of antibody forming cells was measured and the relative avidity of antibody produced determined using a plaque inhibition assay. Splenic lymphocytes from young animals of a non-autoimmune strain (CBA/J) were shown to be capable of generating anti-ssDNA IgM antibody-forming cells in culture which displayed a higher avidity for antigen than that from autoimmune-prone or frankly autoimmune mice. Since an increased switching from IgM to IgG autoantibody production and defects in Fc-mediated signalling by IgG antibody have been identified in autoimmunity, we suggest that the metabolic block, normally in force in non-autoimmune-prone animals, accounts for this elevated avidity of IgM autoantibody. |
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Keywords: | regulation of antibody responses immunoregulation regulation by Fc signals end product feedback self-non-self discrimination |
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