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International Immunology Advance Access originally published online on March 19, 2009
International Immunology 2009 21(5):533-541; doi:10.1093/intimm/dxp024
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© The Japanese Society for Immunology. 2009. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Enhanced capture of extramembranous IgM and IgG on B cells in the NOD mouse—implications for immune complex trapping

Rifat Ekici*, Mia Sundström*, Bernard Thay and Kristina Lejon

Department of Clinical Microbiology, Division of Immunology, Umeå University, SE-901 87 Umeå, Sweden

Correspondence to: K. Lejon; E-mail: kristina.lejon{at}climi.umu.se

Binding of various antibody isotypes to B cells through either Fc{gamma}Rs 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 x 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.

Keywords: antibodies, autoimmunity, diabetes, immune complex, rodent

* These authors contributed equally to this work.

Transmitting editor: J. Ravetch

Received 7 May 2008, accepted 13 February 2009.


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