IL-23 Promotes a Coordinated B Cell Germinal Center Program for Class-Switch Recombination to IgG2b in BXD2 Mice.

作者: Huixian Hong , Min Gao , Qi Wu , PingAr Yang , Shanrun Liu

DOI: 10.4049/JIMMUNOL.2000280

关键词: Downregulation and upregulationB cellPopulationPlasma cellMolecular biologyImmunoglobulin class switchingChemistryGerminal centerTranscriptomeT helper cell

摘要: IL-23 promotes autoimmune disease, including Th17 CD4 T cell development and autoantibody production. In this study, we show that a deficiency of the p19 component in BXD2 (BXD2-p19-/- ) mouse leads to shift follicular helper program from (Tfh)-IL-17 Tfh-IFN-γ. Although germinal center (GC) size number GC B cells remained same, BXD2-p19-/- mice exhibited lower class-switch recombination (CSR) cells, leading serum levels IgG2b. Single-cell transcriptomics analysis revealed whereas Ifngr1, Il21r, Il4r genes synchronized expression pattern with Cxcr5 plasma genes, Il17ra Cxcr4 genes. Downregulation Ighg2b was associated decreased CSR-related novel base excision repair were otherwise predominantly expressed by + mice. Together, these results suggest although is dispensable for formation, it essential promote population Tfh-IL-17 cells. acts indirectly on facilitate during dark zone phase development.

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