Grant: Travel Awards - Institute Community Support

Psoriatic arthritis (PsA) is a chronic inflammatory disease that affects the joints and causes pain, stiffness, and long-term damage. While research has uncovered the role of certain immune cells in driving PsA, the contribution of natural killer (NK) cells, a key part of the body's innate immune system, remains poorly understood. NK cells can directly destroy stressed or damaged cells and release signals that influence other immune cells, bridging innate and adaptive immunity. Studies in PsA patients show reduced NK cell numbers in the blood, but NK cells in affected joints often display an overactive state. Prolonged activation may eventually exhaust these cells, reducing their ability to control inflammation and allowing the disease to persist. A signaling molecule called TNF-alpha, already targeted by common PsA therapies, appears to regulate NK cell activation and exhaustion, making it a critical focus for understanding disease mechanisms. My research aims to clarify how NK cells contribute to PsA and how TNF-alpha influences their function. Using a mouse model, I will define the types and activity states of NK cells, investigate how TNF-alpha signaling affects their behavior, and identify NK cell subtypes and pathways linked to disease severity and treatment response. This work will provide new insights into the immune mechanisms driving PsA, potentially revealing novel therapeutic targets and strategies to better control inflammation and improve patient outcomes.