New mechanism found in psoriatic arthritis treatment

Researchers have found a new mechanism that plays a significant role in psoriatic arthritis (PsA). The study focuses on the tumor necrosis factor-alpha receptor 2 (TNFR2) and its interaction with dendritic cells, which are key players in the immune system. This discovery may lead to new treatment strategies. The team from the Husni laboratory demonstrated that removing TNFR2 from certain immune cells greatly reduces symptoms similar to psoriasis in mouse models. This suggests that TNFR2 has an important role in driving inflammation in psoriatic diseases. When TNFR2 is absent, the number of dendritic cells in the body’s lymphoid organs also decreases. Dendritic cells activate the immune response and have been linked to various inflammatory diseases, including PsA. The study indicates that TNFR2 helps trigger PsA-like inflammation by activating a specific type of dendritic cell known as cDC1. These activated cells produce substances that lead to the activation of T cells, which contribute to the disease. In experiments with genetically modified mice that lacked TNFR2 in dendritic cells, the researchers observed much less inflammation and fewer skin symptoms after they induced PsA. The mice with TNFR2 intact showed severe symptoms, while the modified mice had significantly lower inflammation scores. The findings highlight the importance of the TNFR2/cDC1 pathway in the progression of PsA. Targeting this specific mechanism could lead to more effective and safer treatments. Instead of using broad anti-TNF therapies, which can have unwanted side effects, focused treatments could reduce PsA symptoms while maintaining necessary immune functions. This research opens up new possibilities for treating psoriatic diseases and could greatly improve the quality of life for patients in the future.