| First Author | Hong H | Year | 2020 |
| Journal | J Immunol | Volume | 205 |
| Issue | 2 | Pages | 346-358 |
| PubMed ID | 32554431 | Mgi Jnum | J:291778 |
| Mgi Id | MGI:6445018 | Doi | 10.4049/jimmunol.2000280 |
| Citation | Hong H, et al. (2020) IL-23 Promotes a Coordinated B Cell Germinal Center Program for Class-Switch Recombination to IgG2b in BXD2 Mice. J Immunol 205(2):346-358 |
| abstractText | 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 of IL-23 in the autoimmune BXD2 (BXD2-p19(-/-) ) mouse leads to a shift of the follicular T helper cell program from follicular T helper (Tfh)-IL-17 to Tfh-IFN-gamma. Although the germinal center (GC) size and the number of GC B cells remained the same, BXD2-p19(-/-) mice exhibited a lower class-switch recombination (CSR) in the GC B cells, leading to lower serum levels of IgG2b. Single-cell transcriptomics analysis of GC B cells revealed that whereas Ifngr1, Il21r, and Il4r genes exhibited a synchronized expression pattern with Cxcr5 and plasma cell program genes, Il17ra exhibited a synchronized expression pattern with Cxcr4 and GC program genes. Downregulation of Ighg2b in BXD2-p19(-/-) GC B cells was associated with decreased expression of CSR-related novel base excision repair genes that were otherwise predominantly expressed by Il17ra (+) GC B cells in BXD2 mice. Together, these results suggest that although IL-23 is dispensable for GC formation, it is essential to promote a population of Tfh-IL-17 cells. IL-23 acts indirectly on Il17ra (+) GC B cells to facilitate CSR-related base excision repair genes during the dark zone phase of GC B cell development. |
