Abstract
Binding of various antibody isotypes to B cells through either FcγRs or complement receptors has been attributed to play several roles, e.g. in immune complex (IC) transportation and regulation of B cell receptor signaling. We have revealed a novel B cell intrinsic receptor for IgM and IgG which is present in C57BL/6 (B6) mice and is more abundant in non-obese diabetic (NOD) mice. As a consequence, the level of extramembranous IgG monomers and IgM pentamers on peripheral blood B cells from NOD mice was significantly higher compared with B6 mice. The effect of this aberration was that all B cells in peripheral blood of (NOD.IgHa × B6(IgHb))F1 mice carried both IgM allotypes on their surface. In addition, analysis of IC binding using IgG- or IgM-opsonized bacterial particles revealed a higher degree of binding in NOD mice compared with B6. We hypothesize that this novel Ig-binding receptor is part of the normal immune system function. The aberrant function in the NOD mouse could contribute to the development of Type 1 diabetes by altering normal B cell functions such as activation, IC transportation and B cell homeostasis. © The Japanese Society for Immunology. 2009. All rights reserved.
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Ekici, R., Sundström, M., Thay, B., & Lejon, K. (2009). Enhanced capture of extramembranous IgM and IgG on B cells in the NOD mouse - Implications for immune complex trapping. International Immunology, 21(5), 533–541. https://doi.org/10.1093/intimm/dxp024
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