First Author | Wang Y | Year | 2017 |
Journal | Nat Immunol | Volume | 18 |
Issue | 8 | Pages | 921-930 |
PubMed ID | 28650481 | Mgi Jnum | J:258171 |
Mgi Id | MGI:6141525 | Doi | 10.1038/ni.3788 |
Citation | Wang Y, et al. (2017) Germinal-center development of memory B cells driven by IL-9 from follicular helper T cells. Nat Immunol 18(8):921-930 |
abstractText | Germinal centers (GCs) support high-affinity, long-lived humoral immunity. How memory B cells develop in GCs is not clear. Through the use of a cell-cycle-reporting system, we identified GC-derived memory precursor cells (GC-MP cells) that had quit cycling and reached G0 phase while in the GC, exhibited memory-associated phenotypes with signs of affinity maturation and localized toward the GC border. After being transferred into adoptive hosts, GC-MP cells reconstituted a secondary response like genuine memory B cells. GC-MP cells expressed the interleukin 9 (IL-9) receptor and responded to IL-9. Acute treatment with IL-9 or antibody to IL-9 accelerated or retarded the positioning of GC-MP cells toward the GC edge and exit from the GC, and enhanced or inhibited the development of memory B cells, which required B cell-intrinsic responsiveness to IL-9. Follicular helper T cells (TFH cells) produced IL-9, and deletion of IL-9 from T cells or, more specifically, from GC TFH cells led to impaired memory formation of B cells. Therefore, the GC development of memory B cells is promoted by TFH cell-derived IL-9. |