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Resident Memory T Cells in Autoimmune Skin Diseases

These new findings only reveal a fraction of the relationship between GHR and autophagy

This recognition step triggers further cytokine release and inflammation, thereby perpetuating an inflammationferroptosisinflammation positive feedback loop ( 4.4 Interactions between cartilage and synovium 4.4.1 Interplay between cytokines released by chondrocytes and synovial cells When cartilage is damaged, chondrocytes release proteoglycan fragments, type II collagen fragments, and diverse injury-associated factors that synovial cell surface pattern recognition receptors (PRRs) can detect, prompting synovial hyperplasia and proinflammatory cytokine secretion ( 4.4.2 Synovitis, ferroptosis, and iron homeostasis imbalance Although synovitis is not the primary lesion in OA, its role as a possible inflammatory amplifier cannot be overlooked ( During OA, synovial tissue exhibits an inflammatory response, releasing IL-1, IL-6, TNF-, and other cytokines and chemokines that attract peripheral immune cells such as macrophages, neutrophils, and T cells to the synovial membrane ( As immune cells gather and become activated in the inflamed synovium during OA, ROS production significantly increases

Moreland, K