Protein kinase CK2 enables regulatory T cells to suppress excessive TH2 responses in vivo

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 (T-reg cells). However, how a tissue- and cell type-specific suppressor program of T-reg cells is mechanistically orchestrated has remained largely unexplored. Through the use of T-reg cell-specific gene targeting, we found that the suppression of allergic immune responses in the lungs mediated by T helper type 2 (T(H)2) 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(+) T-reg cell subpopulation that was unable to control the maturation of IRF4(+)PD-L2(+) dendritic cells required for the development of T(H)2 responses in vivo.