| First Author | Jang A | Year | 2021 |
| Journal | Front Immunol | Volume | 12 |
| Pages | 701066 | PubMed ID | 34335611 |
| Mgi Jnum | J:320986 | Mgi Id | MGI:6729442 |
| Doi | 10.3389/fimmu.2021.701066 | Citation | Jang A, et al. (2021) Dependence on Autophagy for Autoreactive Memory B Cells in the Development of Pristane-Induced Lupus. Front Immunol 12:701066 |
| abstractText | The production of autoantibodies by autoreactive B cells plays a major role in the pathogenesis of lupus. Increases in memory B cells have been observed in human lupus patients and autoimmune lpr mice. Autophagy is required for the maintenance of memory B cells against viral infections; however, whether autophagy regulates the persistence of autoantigen-specific memory B cells and the development of lupus remains to be determined. Here we show that memory B cells specific for autoantigens can be detected in autoimmune lpr mice and a pristane-induced lupus mouse model. Interestingly, B cell-specific deletion of Atg7 led to significant loss of autoreactive memory B cells and reduced autoantibody production in pristane-treated mice. Autophagy deficiency also attenuated the development of autoimmune glomerulonephritis and pulmonary inflammation after pristane treatment. Adoptive transfer of wild type autoreactive memory B cells restored autoantibody production in Atg7-deficient recipients. These data suggest that autophagy is important for the persistence of autoreactive memory B cells in mediating autoantibody responses. Our results suggest that autophagy could be targeted to suppress autoreactive memory B cells and ameliorate humoral autoimmunity. |
