■牛皮癣(PsO)是一种由TNFα等免疫介质驱动的慢性皮肤病,INFγ,IL-17和IL-23。银屑病关节炎(PsA)可在PsO患者中发展。虽然银屑病病变可以通过治疗明显消退,亚临床皮肤炎症可能持续存在。组织驻留记忆T细胞(TRM)的作用,和调节性T细胞(Tregs),也有助于慢性炎症在这方面正在探索。这篇系统的综述探讨了TRM和Tregs在银屑病疾病(PsD)中的作用及其进展。
■系统评价,遵循系统审查和荟萃分析(PRISMA)指南的首选报告项目,于2023年6月3日使用Pubmed®和WebofScience™数据库进行,使用患者/人群,干预,比较,和结果(PICO)标准仅限于英语。
■总共确定并包括了62份报告。在PsO,慢性炎症由细胞因子(包括IL-17和IL-23)和细胞介质(如CD8+和CD4+T细胞)驱动。TRM有助于局部炎症,而Tregs可能在银屑病皮肤病变中功能失调。Secukinumab和guselkumab,靶向IL-17A和IL-23p19亚基,分别,PsO处理对CD8+TRM和Tregs有不同的影响。由于IL-23对Treg与CD8+TRM比率的影响,IL-23的抑制可提供更好的长期结果。IL-23甚至在治疗后也可能导致炎症持续。在PsA,亚临床附着性炎被认为是早期发生,Th17细胞参与了这一致病过程。最近的EULAR指南强调了早期诊断和治疗截获PsA的重要性。在PsA,CD8+TRM细胞存在于滑液中,并且Treg在外周血中减少。从PsO到PsA的进展以免疫谱的转变为标志,特定的T细胞亚群在炎症的延续中起着关键作用。针对TRM细胞的早期干预可能有希望,但临床研究有限。正在进行的研究,如IVEPSA和PAMPA旨在提高我们对高风险PsO患者的PsA拦截的认识,强调需要在这一领域进一步研究。
■早期干预对于PsA高风险的PsO患者至关重要;T细胞,特别是17型辅助性T细胞,和CD8+细胞是从PsO到PsA进展的关键。TRM在PsD中的早期靶向显示出希望,但还需要更多的研究。
UNASSIGNED: Psoriasis (PsO) is a chronic skin condition driven by immune mediators like TNFα, INFγ, IL-17, and IL-23. Psoriatic arthritis (PsA) can develop in PsO patients. Although psoriatic lesions may apparently resolve with therapy, subclinical cutaneous inflammation may persist. The role of tissue-resident memory T-cells (TRM), and regulatory T cells (Tregs) that also contribute to chronic inflammation are being explored in this context. This systematic
review explores TRM and Tregs in psoriatic disease (PsD) and its progression.
UNASSIGNED: A systematic
review, following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, was performed using Pubmed® and Web of Science™ databases on June 3rd 2023, using patient/population, intervention, comparison, and outcomes (PICO) criteria limited to the English language.
UNASSIGNED: A total of 62 reports were identified and included. In PsO, chronic inflammation is driven by cytokines including IL-17 and IL-23, and cellular mediators such as CD8+ and CD4+ T cells. TRM contributes to local inflammation, while Tregs may be dysfunctional in psoriatic skin lesions. Secukinumab and guselkumab, which target IL-17A and the IL-23p19 subunit, respectively, have different effects on CD8+ TRM and Tregs during PsO treatment. Inhibition of IL-23 may provide better long-term results due to its impact on the Treg to CD8+ TRM ratio. IL-23 may contribute to inflammation persisting even after treatment. In PsA, subclinical enthesitis is perceived as an early occurence, and Th17 cells are involved in this pathogenic process. Recent EULAR guidelines highlight the importance of early diagnosis and treatment to intercept PsA. In PsA, CD8+ TRM cells are present in synovial fluid and Tregs are reduced in peripheral blood. The progression from PsO to PsA is marked by a shift in immune profiles, with specific T-cells subsets playing key roles in perpetuating inflammation. Early intervention targeting TRM cells may hold promising, but clinical studies are limited. Ongoing studies such as IVEPSA and PAMPA aim to improve our knowledge regarding PsA interception in high-risk PsO patients, emphasizing the need for further research in this area.
UNASSIGNED: Early intervention is crucial for PsO patients at high risk of PsA; T cells, particularly type 17 helper T cells, and CD8+ cells are key in the progression from PsO-to-PsA. Early targeting of TRM in PsD shows promise but more research is needed.