Protein kinase 2 (CK2) controls CD4⁺ T cell effector function in the pathogenesis of colitis.

ABSTRACT: Crohn's disease (CD), one of the major forms of inflammatory bowel disease (IBD), is characterized by chronic inflammation of the gastrointestinal tract and associated with aberrant CD4⁺ T-helper type 1 (Th1) and Th17 responses. Protein kinase 2 (CK2) is a conserved serine-threonine kinase involved in signal transduction pathways, which regulate immune responses. CK2 promotes Th17 cell differentiation and suppresses the generation of Foxp3⁺ regulatory T cells. The function of CK2 in CD4⁺ T cells during the pathogenesis of CD is unknown. We utilized the T cell-induced colitis model, transferring CD45RB^hi-naive CD4⁺ T cells from CK2α^fl/fl controls and CK2α^fl/fldLck-Cre mice into Rag1^-/- mice. CD4⁺

SUBMITTER: Yang W 

PROVIDER: S-EPMC7382987 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature