Fcmr, also known as Toso, is the putative receptor for soluble IgM. It plays a role in regulating the immune system, with implications in immune homeostasis, B cell development, and antigen-driven immune responses [2,3]. It may be involved in pathways related to anti-tumor immunity and autoimmunity [1,4]. Genetic models, such as gene knockout mice, are valuable for studying its functions.

In a syngeneic melanoma model, Fcmr ablation in myeloid cells suppressed tumor growth, increased myeloid cell population density in the malignancy, and enhanced anti-tumor immunity. Fcmr deficiency led to a unique subset of tumor-associated mononuclear phagocytes with enhanced antigen processing/presenting properties. Conversely, Fcmr activity negatively regulated the activation and migratory capacity of myeloid cells in vivo, and T cell activation by bone marrow-derived dendritic cells in vitro [1]. In mouse models, Fcmr-deficient mice had reduced numbers of developing B cells, splenic follicular and peritoneal B-2 cells, but increased levels of peritoneal B-1a cells and autoantibodies. After immunization, germinal center B cell and plasma cell numbers were increased, and Fcmr-deficient B cells were sensitive to apoptosis induced by BCR ligation [3].

In conclusion, Fcmr is crucial for immune-related functions, including B cell differentiation and homeostasis, and the regulation of anti-tumor immunity. Studies using Fcmr KO mouse models have revealed its significance in tumor-related and B-cell-associated disease areas, providing potential therapeutic targets for cancer and insights into autoimmunity mechanisms.