Cellular Mechanisms of Psoriasis Pathogenesis: A Systemic Review.
Mengjun WuChan DaiFanfan ZengPublished in: Clinical, cosmetic and investigational dermatology (2023)
Psoriasis is a common inflammatory skin disease characterized by abnormal proliferation of epidermal keratinocytes and massive infiltration of inflammatory cells. Many kinds of cells, including keratinocytes, T lymphocytes, dendritic cells, neutrophils, and macrophages, are reported to play critical roles in the pathogenesis and progression of psoriasis. However, to date, the role of each kind of cell in the pathogenesis and development of psoriasis has not been systematically reviewed. In addition, although antibodies developed targeting cytokines (e.g. IL-23, IL-17A, and TNF-α) released by these cells have shown promising results in the treatment of psoriasis patients, these targeted antibodies still do not cure psoriasis and only provide short-term relief of symptoms. Furthermore, long-term use of these antibodies has been reported to have adverse physical and psychological effects on psoriasis patients. Therefore, gaining a deeper understanding of the cellular and molecular pathogenesis of psoriasis and providing new thoughts on the development of psoriasis therapeutic drugs is of great necessity. In this review, we summarize the roles of various cells involved in psoriasis, aiming to provide new insights into the pathogenesis and development of psoriasis at the cellular level and hoping to provide new ideas for exploring new and effective psoriasis treatments.
Keyphrases
- induced apoptosis
- dendritic cells
- atopic dermatitis
- end stage renal disease
- cell cycle arrest
- ejection fraction
- oxidative stress
- signaling pathway
- chronic kidney disease
- immune response
- rheumatoid arthritis
- endoplasmic reticulum stress
- physical activity
- stem cells
- drug delivery
- peritoneal dialysis
- regulatory t cells
- combination therapy