Protein kinase CK2 controls T‐cell polarization through dendritic cell activation in response to contact sensitizers

CK2 controls acquisition of a mature phenotype and cytokine production in DCs, allowing Th1 polarization in response to contact sensitizers. Allergic contact dermatitis (ACD) represents a severe health problem with increasing worldwide prevalence. It is a T‐cell‐mediated inflammatory skin disease caused by chemicals present in the daily or professional environment. NiSO4 and 2,4‐dinitrochlorobenzene (DNCB) are 2 chemicals involved in ACD. These contact sensitizers are known to induce an up‐regulation of phenotypic markers and cytokine secretion in dendritic cells (DCs; professional APCs), leading to the generation of CD8+ Tc1/Tc17 and CD4+ Th1/Th17 effector T cells. In the present study, using a peptide array approach, we identified protein kinase CK2 as a novel kinase involved in the activation of human monocyte‐derived DCs (MoDCs) in response to NiSO4 and DNCB. Inhibition of CK2 activity in MoDCs led to an altered mature phenotype with lower expression of CD54, PDL‐1, CD86, and CD40 in response to NiSO4 or DNCB. CK2 activity also regulated proinflammatory cytokine production, such as TNF‐α, IL‐1β, and IL‐23 in MoDCs. Moreover, in a DC/T cell coculture model in an allogeneic setup, CK2 activity in MoDCs played a major role in Th1 polarization in response to NiSO4 and DNCB. CK2 inhibition in MoDCs led to an enhanced Th2 polarization in the absence of contact sensitizer stimulation.