Abstract
Unlike Fc receptors for switched immunoglobulin (Ig) isotypes, Fc receptor for IgM (FcµR) is selectively expressed by lymphocytes. The ablation of the FcµR gene in mice impairs B cell tolerance as evidenced by concomitant production of autoantibodies of IgM and IgG isotypes. In this essay, we reiterate the autoimmune phenotypes observed in mutant mice, ie IgM homeostasis, dysregulated humoral immune responses including autoantibodies, and Mott cell formation. We also propose the potential phenotypes in individuals with FCMR deficiency and the model for FcµR-mediated regulation of self-reactive B cells.
Acknowledgements
We thank Dr. Paolo Casali for providing this opportunity, Dr. Jürgen Wienands for valuable comments, Mr. Hilmar Fünning for literature support, and Mr. Hilmar Frank for informatics support. Some data described in this essay were indebted to the collaboration with Drs. Yusuke Suzuki, Hiroshi Ohno, Yoshiki Kubagawa, Christopher Skopnik, Uwe Klemn, Kyeong-Hee Lee, Nicole Baumgarth, Nikles Engels, and Jürgen Wienands.
Disclosure statement
No potential conflict of interest was reported by the author(s).