Therapeutic Advancements in the Management of Psoriasis: A Clinical Overview and UpdateQasem, Ashkanani, Ali
Cureus (2025) 17 (2), e79097
Abstract: Psoriasis is an autoimmune chronic inflammatory skin condition with a strong genetic predisposition. Pathogenesis of psoriasis is complex and multifactorial; it is known that genetic, immunological, and environmental factors play significant roles in its development. Treatment options vary and include topical therapy (e.g., corticosteroids, vitamin D analogs, and calcineurin inhibitors), phototherapy (e.g., narrowband ultraviolet radiation (NB-UVB)), and systemic therapy (e.g., methotrexate and retinoids). Several new treatments have emerged in recent years, including biological treatments. Biologics approved by the United States Food and Drug Administration (FDA) for the treatment of psoriasis include inhibitors of tumor necrosis factor (TNF)-α. Other FDA-approved biologics for the treatment of psoriasis target cytokines, such as the p40 subunit of interleukin (IL)-12 and IL-23, IL-17, as well as the p19 subunit of IL-23. Additionally, the Janus kinase (JAK) inhibitor deucravacitinib is also FDA-approved for the treatment of moderate-to-severe psoriasis. Other promising treatment modalities are consistently undergoing trials. Further therapeutic details, including regimens, side effects, indications, contraindications, and FDA approval dates, are discussed comprehensively in this article. For the purpose of this review, the literature was thoroughly searched for publications discussing psoriasis therapy. This review aims to provide a comprehensive overview and update on the management of psoriasis.Copyright © 2025, Qasem et al.
Mucosal-associated invariant T-cells in pulmonary pathophysiologyKamiki, Gorgulho, Lérias
et alCurr Opin Pulm Med (2025)
Abstract: Mucosal-associated invariant T-cells (MAIT) have been associated with lung cancer and pulmonary infections. The treatment of patients with cancer or infections includes host-directed therapies (HDTs). MAIT play a role in shaping the 'milieu interne' in cancer and infections and this review addresses the biology of MAIT in pulmonary pathophysiology.MAIT represent an attractive target for therapy in pulmonary malignancies and infections. T-cells are often difficult to exploit therapeutically due to the diversity of both T-cell receptor (TCR) repertoire and its ligandome. MAIT-cells are restricted by the major histocompatibility complex class I-related gene protein (MR1) that presents nondefined tumor-associated targets, bacterial products, vitamin and drug derivates. Due to their plasticity in gene expression, MAIT are able to conversely switch from IFN-γ to IL-17 production. Both cytokines play a key role in protective immune responses in infections and malignancies. MAIT-derived production of interleukin (IL)-17/TGF-β shapes the tumor micro-environment (TME), including tissue re-modelling leading to pulmonary fibrosis and recruitment of neutrophils. MAIT contribute to the gut-lung axis associated with clinical improved responses of patients with cancer to checkpoint inhibition therapy. MAIT are at the crossroad of HDTs targeting malignant and infected cells. Clinical presentations of overt inflammation, protective immune responses and tissue re-modeling are reviewed along the balance between Th1, Th2, Th9, and Th17 responses associated with immune-suppression or protective immune responses in infections.MAIT shape the TME in pulmonary malignancies and infections. Drugs targeting the TME and HDTs affect MAIT that can be explored to achieve improved clinical results while curbing overt tissue-damaging immune responses.Copyright © 2025 The Author(s). Published by Wolters Kluwer Health, Inc.
Ethyl acetate extract from Herpetospermun cardigerum wall. Ameliorated concanavalin A-induced autoimmune hepatitis in mice by reprofiling gut microenvironment to modulate IDO1/KYN and PI3K/AKT/NF-κB pathwaysXiao, Luo, Duan
et alJ Ethnopharmacol (2025) 345, 119578
Abstract: Autoimmune hepatitis (AIH) is an immunoinflammatory chronic liver disease with increasing prevalence worldwidely, lacking of effective medicine. Herpetospermum caudigerum Wall. (HC) is a traditional Tibetan medicine used to treat liver diseases for thousands of years. However, investigation into the effects of HC in AIH remains scarce.Our study aimed to explore the effects and mechanisms of ethyl acetate extract from the seeds of HC (HCDEAE) against concanavalin A (Con A)-induced liver impairment in mouse.HCDEAE was extracted from the seeds of HC, then characterized by UPLC-Q-TOF/MS. Con A-induced AIH mice were used to investigate the impacts of HCDEAE on liver impairment, T cells differentiation, gut microbiota and its derived metabolites, intestinal barrier impairment and inflammation, as well as the mechanisms of HCDEAE in liver in AIH.HCDEAE (90 mg/kg, i.g.) effectively alleviated Con A-induced hepatic pathological damage, suppressed elevation of serum ALT, AST, IFN-γ, and TNF-α; in spleen, HCDEAE attenuated spleen impairment, elevated the percentage of CD4+CD25+ cells and FOXP3 gene expression, inhibited up-regulation of RORγt gene expression and IL-17; in liver, HCDEAE down-regulated IL-17, elevated FOXP3 gene expression and IL-10, increased the protein and gene expression of TGF-β1; in colon, HCDEAE attenuated intestinal barrier impairment, inhibited down-regulation of Occludin and ZO-1, and relieved elevation of IL-1β, as well as re-profiled the gut microenvironment. Furthermore, HCDEAE demonstrated the ability to elevate tryptophan metabolism among kynurenine pathway, activate IDO1/KYN pathway and inhibit PI3K/AKT/NF-κB signaling pathway in liver of AIH mice.Pretreatment with HCDEAE (90 mg/kg·d-1, i.g.) for 9 days could effectively alleviate the liver inflammation and injure, protect intestinal barriers, attenuate spleen impairment, maintain Treg-Th17 cell equilibrium in Con A-induced AIH mice, via re-profiling gut microbiota, modulation of tryptophan metabolism in the gastrointestinal tract and in liver, to activate IDO1/KYN pathway and inhibit the abnormal activation of PI3K/AKT/NF-κB signaling pathway in liver. The present study highlighted the potential of HCDEAE as a drug candidate for AIH.Copyright © 2025 Elsevier B.V. All rights reserved.
Protective effects of Rosa roxburghii Tratt. extract against UVB-induced inflammaging through inhibiting the IL-17 pathwayZhang, Chen, Qu
Sci Rep (2025) 15 (1), 8260
Abstract: Chronic inflammation is a critical mechanism contributing to the aging process; however, research specifically addressing chronic inflammation in skin biology remains limited. This study investigates the protective mechanism of Rosa roxburghii Tratt. (RRT) extract against UVB-induced inflammaging. RRT extract effectively reduces the secretion of IL-6, IL-1α, TNF-α, and PGE2 in keratinocytes. Additionally, it attenuates UVB-induced IL-17 pathway activation by downregulating IL-17RA, c-Fos, and c-Jun protein levels, as well as the gene expression of IL-17RA, TRAF6, HSP90, and IKKγ. Co-culturing human foreskin fibroblasts (HFF) with inflammatory factors secreted by UVB-exposed keratinocytes reveals that these factors significantly reduce mitochondrial membrane potential and mitochondrial reactive oxygen species (ROS), thereby promoting aging in HFF. The anti-inflammaging effects of RRT extract are achieved through the reduction of β-galactosidase activity, targeting of the TGF-β1-Smad2/3 signaling pathway, upregulation of COL1A1 expression, and reduction of senescence-associated secretory phenotype secretion. This study provides a novel perspective and robust scientific foundation for exploring mechanisms of skin aging and potential therapeutic interventions.© 2025. The Author(s).
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