Safety of exercise after pulmonary endarterectomy: a systematic review.

Psoriasis is a chronic immune-mediated skin disorder characterized by complex interactions among dendritic cells, Th1/Th2/Th17 cells, and B cells, which collectively drive keratinocyte proliferation and sustained cutaneous inflammation. Type 1 immune responses (Th1/IFN-γ) primarily mediate cell-mediated immunity, while Type 2 immune responses (Th2/IL-4, IL-13) contribute to humoral immunity, and Th17/IL-17 pathways play a central role in amplifying local and systemic inflammation. Psoriasis is driven by the coordinated activity of dendritic cells, Th1, Th2, Th17 cells, and B cells, which collectively promote keratinocyte hyperproliferation and persistent cutaneous inflammation. Type 1 immune responses (Th1/IFN-γ) mediate cell-mediated immunity, Type 2 responses (Th2/IL-4, IL-13) drive humoral immunity, and Th17/IL-17 pathways amplify local and systemic inflammation. Psoriasis also affects all aspects of the patient’s quality of life, including emotional well-being; thus, depression, anxiety, and sleep problems are frequently reported among individuals with psoriasis (–). In recent years, there has been growing evidence describing the biological and clinical links between psoriasis and psychiatric disorders. Early literature discussed epidemiological findings and psychosocial consequences of mobilizing psoriasis; however, emerging data indicate that systemic inflammation, HPA axis dysregulation, and microglial activation within specific brain regions (hippocampus, prefrontal cortex) may contribute to psychiatric comorbidity, with cytokine-mediated neural modulation supported by both clinical biomarker studies and preclinical animal models (–). Causal interpretations remain cautious, as human studies are primarily correlational. The role of HPA axis dysregulation and neuroinflammatory processes in psychiatric symptoms in chronic inflammatory disease has generated interest in integrated dermatological and psychiatric care ().