Document Type : Review Article
Authors
1
Department of Medical Biochemistry , Faculty of Medicine , Sohag university , Sohag , Egypt
2
Deparment of Physical Medicine Rheumatology and Rehabilitation
3
Physiology ,Faculty of medicine, Sohag University
4
Community medicine, faculty of medicine, Sohag university, Sohag, Egypt
5
Department of Dermatology, Faculty of medicine, Sohag University, Sohag, Egypt
6
forensic medicine and clinical toxicology department, faculty of medicine, sohag university
Abstract
Psoriasis is a chronic inflammatory skin condition marked by scaly, hardened red plaques, which extend beyond the skin to affect joints and nails. It is often associated with systemic, psychiatric, and psychosocial disorders. Keratinocytes are fundamental in both initiating and maintaining psoriasis as part of the body's innate immune response. These skin cells can react to various environmental stimuli. When stressed, keratinocytes release self-nucleotides and antimicrobial peptides, which in turn activate plasmacytoid dendritic cells (pDCs). This leads to the activation and maturation of myeloid dendritic cells (mDCs), which produce pro-inflammatory cytokines such as IFN-α, IFN-γ, TNF-α, and IL-1β Vitamin D helps maintain the health of the skeletal system and epidermis, regulating keratinocyte differentiation and proliferation. There is a strong connection between vitamin D and the IL-33/ST2 axis in regulating skin and bone homeostasis. This review explores the bidirectional interactions between vitamin D and psoriasis, suggesting a mechanistic link with IL-33 in patients suffering from psoriasis and related osteoporosis (OP).
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