Targeting dendritic cell-specific TNFR2 improves skin and joint inflammation in a murine model of psoriatic arthritis.

ABSTRACT: Psoriasis (PsO) and Psoriatic arthritis (PsA) are TNF-alpha-dependent immune-mediated inflammatory diseases where dendritic cells (DC) play a critical role in disease pathogenesis. Although TNF-alpha receptor 2 (TNFR2) has been implicated in the pathology of psoriatic diseases, its specific role in DC mediated responses remains unclear. To investigate the role of TNFR2 in DC in psoriatic disease, we utilized the mannan-oligosaccharide (MOS) model of PsA on mice with either TNFR2 intact or with DC-specific TNFR2 knockout (DC-TNFR2KO). We evaluated disease severity by assessing skin scaling, joint inflammation, serum cytokine profiles, and changes in the conventional type 1 dendritic cell (cDC1) population. A significant reduction in PsA-like skin scaling and joint inflammation was observed

SUBMITTER: Kaur R 

PROVIDER: S-EPMC12391354 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature