| First Author | Ono C | Year | 2023 |
| Journal | Front Immunol | Volume | 14 |
| Pages | 1276014 | PubMed ID | 37841260 |
| Mgi Jnum | J:344088 | Mgi Id | MGI:7541986 |
| Doi | 10.3389/fimmu.2023.1276014 | Citation | Ono C, et al. (2023) Upregulated Fcrl5 disrupts B cell anergy causes autoimmune disease. Front Immunol 14:1276014 |
| abstractText | B cell anergy plays a critical role in maintaining self-tolerance by inhibiting autoreactive B cell activation to prevent autoimmune diseases. Here, we demonstrated that Fc receptor-like 5 (Fcrl5) upregulation contributes to autoimmune disease pathogenesis by disrupting B cell anergy. Fcrl5-a gene whose homologs are associated with human autoimmune diseases-is highly expressed in age/autoimmunity-associated B cells (ABCs), an autoreactive B cell subset. By generating B cell-specific Fcrl5 transgenic mice, we demonstrated that Fcrl5 overexpression in B cells caused systemic autoimmunity with age. Additionally, Fcrl5 upregulation in B cells exacerbated the systemic lupus erythematosus-like disease model. Furthermore, an increase in Fcrl5 expression broke B cell anergy and facilitated toll-like receptor signaling. Thus, Fcrl5 is a potential regulator of B cell-mediated autoimmunity by regulating B cell anergy. This study provides important insights into the role of Fcrl5 in breaking B cell anergy and its effect on the pathogenesis of autoimmune diseases. |
