| First Author | Ulges A | Year | 2015 |
| Journal | Nat Immunol | Volume | 16 |
| Issue | 3 | Pages | 267-75 |
| PubMed ID | 25599562 | Mgi Jnum | J:259002 |
| Mgi Id | MGI:6140962 | Doi | 10.1038/ni.3083 |
| Citation | Ulges A, et al. (2015) Protein kinase CK2 enables regulatory T cells to suppress excessive TH2 responses in vivo. Nat Immunol 16(3):267-75 |
| abstractText | The quality of the adaptive immune response depends on the differentiation of distinct CD4(+) helper T cell subsets, and the magnitude of an immune response is controlled by CD4(+)Foxp3(+) regulatory T cells (Treg cells). However, how a tissue- and cell type-specific suppressor program of Treg cells is mechanistically orchestrated has remained largely unexplored. Through the use of Treg cell-specific gene targeting, we found that the suppression of allergic immune responses in the lungs mediated by T helper type 2 (TH2) cells was dependent on the activity of the protein kinase CK2. Genetic ablation of the beta-subunit of CK2 specifically in Treg cells resulted in the proliferation of a hitherto-unexplored ILT3(+) Treg cell subpopulation that was unable to control the maturation of IRF4(+)PD-L2(+) dendritic cells required for the development of TH2 responses in vivo. |
