de Jesús-Gil Carmen, Sans-de San Nicolàs Lídia, García-Jiménez Irene, Ferran Marta, Pujol Ramon M, Santamaria-Babí Luis F
Translational Immunology, Department of Cellular Biology, Physiology and Immunology, Faculty of Biology, Universitat de Barcelona, Parc Científic de Barcelona, Barcelona, Spain.
Department of Dermatology, Hospital del Mar (Institut Hospital del Mar d'Investigacions Mèdiques), Universitat Autònoma de Barcelona, Barcelona, Spain.
Front Med (Lausanne). 2021 Oct 29;8:731911. doi: 10.3389/fmed.2021.731911. eCollection 2021.
Psoriasis is a common inflammatory skin condition resulting from the interplay between epidermal keratinocytes and immunological cellular components. This sustained inflammation is essentially driven by pro-inflammatory cytokines with the IL-23/IL-17 axis playing a critical central role, as proved by the clinical efficacy of their blockade in patients. Among all the CD45R0 memory T cell subsets, those with special tropism for cutaneous tissues are identified by the expression of the Cutaneous Lymphocyte-associated Antigen (CLA) carbohydrate on their surface, that is induced during T cell maturation particularly in the skin-draining lymph nodes. Because of their ability to recirculate between the skin and blood, circulating CLA memory T cells reflect the immune abnormalities found in different human cutaneous conditions, such as psoriasis. Based on this premise, studying the effect of different environmental microbial triggers and psoriatic lesional cytokines on CLA memory T cells, in the presence of autologous epidermal cells from patients, revealed important IL-17 cytokines responses that are likely to enhance the pro-inflammatory loop underlying the development of psoriatic lesions. The goal of this mini-review is to present latest data regarding cytokines implicated in plaque and guttate psoriasis immunopathogenesis from the prism of CLA memory T cells, that are specifically related to the cutaneous immune system.
银屑病是一种常见的炎症性皮肤病，由表皮角质形成细胞和免疫细胞成分之间的相互作用引起。这种持续的炎症主要由促炎细胞因子驱动，其中IL-23/IL-17轴起着关键的核心作用，这已被它们在患者中的阻断治疗的临床疗效所证实。在所有CD45R0记忆T细胞亚群中，那些对皮肤组织具有特殊嗜性的亚群通过其表面皮肤淋巴细胞相关抗原（CLA）碳水化合物的表达来识别，CLA碳水化合物在T细胞成熟过程中尤其是在引流皮肤的淋巴结中诱导产生。由于循环CLA记忆T细胞具有在皮肤和血液之间再循环的能力，它们反映了在不同人类皮肤疾病（如银屑病）中发现的免疫异常。基于这一前提，在存在患者自体表皮细胞的情况下，研究不同环境微生物触发因素和银屑病皮损细胞因子对CLA记忆T细胞的影响，揭示了重要的IL-17细胞因子反应，这些反应可能会增强银屑病皮损发展的促炎循环。本综述的目的是从CLA记忆T细胞的角度，介绍与斑块状和点滴状银屑病免疫发病机制相关的细胞因子的最新数据，这些数据与皮肤免疫系统特别相关。
