Other
12 Authors
- Qi H,
- Kang SG,
- Jin HY,
- Xiao C,
- Oldstone MB,
- Lim HW,
- Fremgen D,
- Verdin E,
- Liu WH,
- Shepherd J,
- Lu P,
- Teijaro JR
First Author | Kang SG | Year | 2013 |
Journal | Nat Immunol | Volume | 14 |
Issue | 8 | Pages | 849-57 |
PubMed ID | 23812097 | Mgi Jnum | J:201798 |
Mgi Id | MGI:5515785 | Doi | 10.1038/ni.2648 |
Citation | Kang SG, et al. (2013) MicroRNAs of the miR-17 approximately 92 family are critical regulators of T(FH) differentiation. Nat Immunol 14(8):849-57 |
abstractText | Follicular helper T cells (T(FH) cells) provide critical help to B cells during humoral immune responses. Here we report that mice with T cell-specific deletion of the miR-17 approximately 92 family of microRNAs (miRNAs) had substantially compromised T(FH) differentiation, germinal-center formation and antibody responses and failed to control chronic viral infection. Conversely, mice with T cell-specific expression of a transgene encoding miR-17 approximately 92 spontaneously accumulated T(FH) cells and developed a fatal immunopathology. Mechanistically, the miR-17 approximately 92 family controlled the migration of CD4(+) T cells into B cell follicles by regulating signaling intensity from the inducible costimulator ICOS and kinase PI(3)K by suppressing expression of the phosphatase PHLPP2. Our findings demonstrate an essential role for the miR-17 approximately 92 family in T(FH) differentiation and establish PHLPP2 as an important mediator of their function in this process. |