First Author | Boucheron N | Year | 2010 |
Journal | J Immunol | Volume | 185 |
Issue | 9 | Pages | 5111-9 |
PubMed ID | 20870948 | Mgi Jnum | J:165197 |
Mgi Id | MGI:4836434 | Doi | 10.4049/jimmunol.1001734 |
Citation | Boucheron N, et al. (2010) The protein tyrosine kinase Tec regulates a CD44highCD62L- Th17 subset. J Immunol 185(9):5111-9 |
abstractText | The generation of Th17 cells has to be tightly controlled during an immune response. In this study, we report an increase in a CD44(high)CD62L(-) Th17 subset in mice deficient for the protein tyrosine kinase Tec. CD44(high)CD62L(-) Tec(-/-) CD4(+) T cells produced enhanced IL-17 upon activation, showed increased expression levels of IL-23R and RORgammat, and IL-23-mediated expansion of Tec(-/-) CD4(+) T cells led to an increased production of IL-17. Tec(-/-) mice immunized with heat-killed Streptococcus pneumoniae displayed increased IL-17 expression levels in the lung postinfection with S. pneumoniae, and this correlated with enhanced pneumococcal clearance and reduced lung inflammation compared with Tec(+/+) mice. Moreover, naive Tec(-/-) OT-II CD4(+) T cells produced higher levels of IL-17 when cultured with OVA peptide-loaded bone marrow-derived dendritic cells that have been previously activated with heat-killed S. pneumoniae. Taken together, our data indicated a critical role for Tec in T cell-intrinsic signaling pathways that regulate the in vivo generation of CD44(high)CD62L(-) effector/memory Th17 populations. |