Protein kinase CK2 enables regulatory T cells to suppress excessive TH2 responses in vivo
Alexander Ulges, Matthias Klein, Sebastian Reuter, Bastian Gerlitzki, Markus Hoffmann, Nadine Grebe, Valérie Staudt, Natascha Stergiou, Toszka Bohn, Till-Julius Brühl, Sabine Muth, Hajime Yurugi, Krishnaraj Rajalingam, Iris Bellinghausen, Andrea Tuettenberg, Susanne Hahn, Sonja Reißig, Irma Haben, Frauke Zipp, Ari Waisman, Hans-Christian Probst, Andreas Beilhack, Thierry Buchou, Odile Filhol-Cochet, Brigitte Boldyreff et al.
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 β-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.
