Dependence on Autophagy for Autoreactive Memory B Cells in the Development of Pristane-Induced Lupus

Albert Jang, Robert Sharp, Jeffrey Wang, Yin Feng, Jin Wang, Min Chen

Research output: Contribution to journalArticlepeer-review

Abstract

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.
Original languageEnglish (US)
Article number701066
Pages (from-to)1-14
Number of pages14
JournalFrontiers in immunology
Volume12
DOIs
StatePublished - Jul 16 2021

Keywords

  • autoantibody; autophagy; autoreactive memory B cells; glomerulonephritis; lupus; memory B cells; pristane induced lupus; systemic autoimmunity.

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