PLX193307

GSE124885: A CD4 T cell population expand and reshape autoreactive B cells, contributing to autoimmune lung pathology and post-infection autoimmunity in children

• Organsim mouse
• Type RNASEQ
• Target gene
• Project ARCHS4

Community acquired pneumonia (CAP) is a significant risk factor for autoimmune disease development. However, mechanisms underlying infection and autoimmunity remain elusive. Here, we report selective expansion of autoantibody producing CD21-CD19+ B cells by bronchoalveolar PD-1+CCR2+GZMA+RUNX3+ T helper 1 like (aTh1) cells in children with CAP. In bronchoalveolar lavage, the numbers of aTh1, CD21-B cells and the concentrations of IgG-specific autoantibodies correlated with CAP severity. Unexpectedly, PD-1 decreased the ability of CD21- B cells to produce autoantibodies and reshaped their specificity in the course of pathogen invasion. Nevertheless, respiratory infection induced aTh1 and CD21-B cell persistence may trigger autoimmune disease development in susceptible individuals; e.g. they were prevalent in cerebrospinal fluid of children with post-infection Guillain-Barre Syndrome. Thus, we reveal dual roles of aTh1 and CD21-B cells in infection immunity and autoimmune pathology, and demonstrate that PD-1 is a critical checkpoint inhibitor for autoimmune disease development. SOURCE: Yuxia Zhang (yuxia.zhang@gwcmc.org) - Zhang Lab Guangzhou Women and Children's Medical Center