| First Author | Tiller T | Year | 2010 |
| Journal | J Exp Med | Volume | 207 |
| Issue | 12 | Pages | 2767-78 |
| PubMed ID | 21078890 | Mgi Jnum | J:176871 |
| Mgi Id | MGI:5292841 | Doi | 10.1084/jem.20100171 |
| Citation | Tiller T, et al. (2010) Development of self-reactive germinal center B cells and plasma cells in autoimmune Fc gammaRIIB-deficient mice. J Exp Med 207(12):2767-78 |
| abstractText | Abnormalities in expression levels of the IgG inhibitory Fc gamma receptor IIB (FcgammaRIIB) are associated with the development of immunoglobulin (Ig) G serum autoantibodies and systemic autoimmunity in mice and humans. We used Ig gene cloning from single isolated B cells to examine the checkpoints that regulate development of autoreactive germinal center (GC) B cells and plasma cells in FcgammaRIIB-deficient mice. We found that loss of FcgammaRIIB was associated with an increase in poly- and autoreactive IgG(+) GC B cells, including hallmark anti-nuclear antibody-expressing cells that possess characteristic Ig gene features and cells producing kidney-reactive autoantibodies. In the absence of FcgammaRIIB, autoreactive B cells actively participated in GC reactions and somatic mutations contributed to the generation of highly autoreactive IgG antibodies. In contrast, the frequency of autoreactive IgG(+) B cells was much lower in spleen and bone marrow plasma cells, suggesting the existence of an FcgammaRIIB-independent checkpoint for autoreactivity between the GC and the plasma cell compartment. |
