| First Author | Ekici R | Year | 2009 |
| Journal | Int Immunol | Volume | 21 |
| Issue | 5 | Pages | 533-41 |
| PubMed ID | 19299625 | Mgi Jnum | J:148104 |
| Mgi Id | MGI:3843546 | Doi | 10.1093/intimm/dxp024 |
| Citation | Ekici R, et al. (2009) Enhanced capture of extramembranous IgM and IgG on B cells in the NOD mouse--implications for immune complex trapping. Int Immunol 21(5):533-41 |
| abstractText | Binding of various antibody isotypes to B cells through either FcgammaRs 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.IgH(a) x B6(IgH(b)))F(1) 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. |
