Lanying Wang

Psoriasis is a chronic inflammatory autoimmune skin disease significantly impairing the patients’ quality of life. Keratin (K)14 and K17 are abnormally expressed in psoriasis patients and considered to be potential autoantigens triggering this disease. However, the animal model for psoriasis induced with a specific antigen is yet to be established. Here we show that vaccinating BALB/c and C57BL/6J mice with purified murine recombinant K14 or K17 antigen induced psoriasis-like clinical symptoms in 40 ± 30% of animals, such as erythema and scaling, accompanied by hallmark histopathological changes including significant epidermal hyperplasia and inflammatory cell infiltration in the lesions. Furthermore, the immunized mice produced high levels of specific antibodies against K14/K17 in the blood, along with antigen-specific T-cell responses. These data indicate that immunization of mice with K14 and K17 antigens could cause psoriasis-like symptoms with immunopathological features of psoriasis, providing a novel experimental animal model for investigating the pathogenesis of psoriasis and development of effective therapies.

Psoriasis is a chronic inflammatory autoimmune skin disease characterized by erythematous plaques covered with silvery-white scales, often accompanied by systemic complications such as psoriatic arthritis and cardiovascular diseases. The disease and its systemic complications substantially impair quality of life, compromise socioeconomic status, and threaten patient safety. The occurrence and progression of this disease are related to the IL-23/IL-17 axis and involve the aberrant activation and interactions of multiple immune cells, along with genetic predispositions and environmental triggers. Although current therapeutic approaches, including topical agents, systemic medications, biologic agents targeting key cytokines, and Janus Kinase inhibitors, can control symptoms and delay disease progression, a complete cure has not been achieved. Furthermore, these strategies face challenges relating to the cost, safety, efficacy and precision of targeting. This review summarizes recent advances in mechanistic research, highlighting the interplay among microorganisms, innate and adaptive immunity in psoriasis. We also evaluate a range of emerging therapies, including biologics, small-molecule inhibitors, Chimeric antigen receptor T-cell cell therapy, RNA interference-based strategies, and alternative medicine. Specifically, we focus on their novel mechanisms, efficacy challenges, safety profiles, and targeting accuracy. Finally, we assess their potential in personalized treatment, aiming to achieve long-term remission, and propose the future prospects of precision medicine in psoriasis management.

Psoriasis is a chronic inflammatory autoimmune skin disease characterized by erythematous plaques covered with silvery-white scales, often accompanied by systemic complications such as psoriatic arthritis and cardiovascular diseases. The occurrence and progression of this disease are related to the IL-23/IL-17 axis and involve aberrant activation and interactions of multiple immune cells, including keratinocytes, dendritic cells, Th17 cells, and neutrophils, with genetic predispositions and environmental triggers. Currently, psoriasis remains incurable. Therapeutic strategies that primarily focus on immunosuppression, anti-inflammation, and palliative care can only control and delay disease progression. These strategies face challenges relating to cost, safety, efficacy and precision of targeting. Future research should prioritize individualized treatment, immune tolerance induction, and microbiome modulation to achieve long-term disease control and potential cure. This review is primarily focused on the progress and prospects of the pathogenesis and therapies for psoriasis, aiming to provide new insights for individualized treatment in the future.