Journal
NATURE IMMUNOLOGY
Volume 16, Issue 3, Pages 267-U227Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3083
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Funding
- Deutsche Forschungsgemeinschaft [DFG BO 3306/1-1, SCHM 1014/7-1, SCHM 1014/5-1, SFB TR128, SFB 1066, BR 3754/2-1]
- International Graduate School of Immunotherapy [GRK 1043]
- Forschungszentrum Immunologie of the University Medical Center of the Johannes Gutenberg-University Mainz
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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.
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