| First Author | Song W | Year | 2022 |
| Journal | Immunity | Volume | 55 |
| Issue | 2 | Pages | 290-307.e5 |
| PubMed ID | 35090581 | Mgi Jnum | J:351476 |
| Mgi Id | MGI:6874622 | Doi | 10.1016/j.immuni.2022.01.002 |
| Citation | Song W, et al. (2022) Development of Tbet- and CD11c-expressing B cells in a viral infection requires T follicular helper cells outside of germinal centers. Immunity 55(2):290-307.e5 |
| abstractText | Tbet(+)CD11c(+) B cells arise during type 1 pathogen challenge, aging, and autoimmunity in mice and humans. Here, we examined the developmental requirements of this B cell subset. In acute infection, T follicular helper (Tfh) cells, but not Th1 cells, drove Tbet(+)CD11c(+) B cell generation through proximal delivery of help. Tbet(+)CD11c(+) B cells developed prior to germinal center (GC) formation, exhibiting phenotypic and transcriptional profiles distinct from GC B cells. Fate tracking revealed that most Tbet(+)CD11c(+) B cells developed independently of GC entry and cell-intrinsic Bcl6 expression. Tbet(+)CD11c(+) and GC B cells exhibited minimal repertoire overlap, indicating distinct developmental pathways. As the infection resolved, Tbet(+)CD11c(+) B cells localized to the marginal zone where splenic retention depended on integrins LFA-1 and VLA-4, forming a competitive memory subset that contributed to antibody production and secondary GC seeding upon rechallenge. Therefore, Tbet(+)CD11c(+) B cells comprise a GC-independent memory subset capable of rapid and robust recall responses. |
