| First Author | Takatsuka S | Year | 2018 |
| Journal | Nat Immunol | Volume | 19 |
| Issue | 9 | Pages | 1025-1034 |
| PubMed ID | 30082831 | Mgi Jnum | J:301723 |
| Mgi Id | MGI:6506914 | Doi | 10.1038/s41590-018-0177-0 |
| Citation | Takatsuka S, et al. (2018) IL-9 receptor signaling in memory B cells regulates humoral recall responses. Nat Immunol 19(9):1025-1034 |
| abstractText | Memory B cells (Bmem cells) are the basis of long-lasting humoral immunity. They respond to re-encountered antigens by rapidly producing specific antibodies and forming germinal centers (GCs), a recall response that has been known for decades but remains poorly understood. We found that the receptor for the cytokine IL-9 (IL-9R) was induced selectively on Bmem cells after primary immunization and that IL-9R-deficient mice exhibited a normal primary antibody response but impaired recall antibody responses, with attenuated population expansion and plasma-cell differentiation of Bmem cells. In contrast, there was augmented GC formation, possibly due to defective downregulation of the ligand for the co-stimulatory receptor ICOS on Bmem cells. A fraction of Bmem cells produced IL-9. These findings indicate that IL-9R signaling in Bmem cells regulates humoral recall responses. |
