Abstract
Psoriasis is the result of uncontrolled keratinocyte proliferation, and its pathogenesis involves the dysregulation of the immune system. The interplay among cytokines released by dendritic, Th1, Th2, and Th17 cells leads to the phenotypical manifestations seen in psoriasis. Biological therapies target the cytokine-mediated pathogenesis of psoriasis and have improved patient quality of life. This review will describe the underlying molecular pathophysiology and biologics used to treat psoriasis. A review of the literature was conducted using the PubMed and Google Scholar repositories to investigate the molecular pathogenesis, clinical presentation, and current therapeutics in psoriasis. Plaque psoriasis’, the most prevalent subtype of psoriasis, pathogenesis primarily involves cytokines TNF-α, IL-17, and IL-23. Pustular psoriasis’, an uncommon variant, pathogenesis involves a mutation in IL-36RN. Currently, biological therapeutics targeted at TNF-α, IL-12/IL-23, IL-17, and IL-23/IL-39 are approved for the treatment of moderate to severe psoriasis. More studies need to be performed to elucidate the precise molecular pathology and assess efficacy between biological therapies for psoriasis. Psoriasis is a heterogenous, chronic, systemic inflammatory disease that presents in the skin with multiple types. Recognizing and understanding the underlying molecular pathways and biological therapeutics to treat psoriasis is important in treating this common disease.
Highlights
Psoriasis is a chronic, systemic inflammatory skin disease that affects approximately3% or 7.5 million people in the United States [1–3]
The main Antimicrobial peptides (AMPs) involved in the pathogenesis of psoriasis include LL37, β-defensins, and S100 proteins [1]
The underlying molecular pathogenesis of psoriasis can be divided into an initiation and maintenance phase
Summary
Systemic inflammatory skin disease that affects approximately3% or 7.5 million people in the United States [1–3]. Systemic inflammatory skin disease that affects approximately. Psoriasis has a prevalence of approximately 1.99% in East Asia, 1.92% in Western Europe, and 1.10% in high-income. Psoriasis occurs in both males and females and has a bimodal age of peak occurrence: between 20–30 and 60–70 [5,6]. The underlying pathogenesis of psoriasis results from an interplay between various genetic and environmental factors. Over 80 human leukocyte genes (HLA) are associated with psoriasis, and HLA-C*06:02 has the strongest association [2]. Environmental factors that can trigger psoriasis include trauma, drugs, infections, smoking, alcohol, and stress. Certain drugs that can exacerbate psoriasis include antimalarials, bupropion, beta-blockers, calcium channel blockers, captopril, and fluoxetine [7]. Scratching, and other forms of trauma, are associated with the onset of psoriasis, known formally as Koebner’s phenomenon [3]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
