Localized cutaneous leishmaniasis (LCL) caused by Leishmania (Viannia) panamensis is an endemic disease in Panama. This condition causes ulcerated skin lesions characterized by a mixed Th1/Th2 immune response that is responsible for disease pathology. However, the maintenance of the in situ inflammatory process involves other elements, such as Th17 and inflammasome responses. Although these processes are associated with parasite elimination, their role in the increase in disease pathology cannot be discarded. Thus, the role in Leishmania infection is still unclear. In this sense, the present study aimed at characterizing the Th17 and inflammasome responses in the skin lesions of patients with LCL caused by L. (V.) panamensis to help elucidate the pathogenesis of this disease in Panama. Th17 and inflammasome responses were evaluated by immunohistochemistry (IHQ) in 46 skin biopsies from patients with LCL caused by L. (V.) panamensis. The Th17 immune response was assessed using CD3, CD4, RoRγt, IL-17, IL-6, IL-23, and TGF-β1 antibodies, and the inflammasome response was assessed by IL-1β, IL-18, and caspase-1 antibodies. The presence of the Th17 and inflammasome responses was evidenced by a positive reaction for all immunological markers in the skin lesions. An inverse correlation between the density of amastigotes and the density of RoRγt⁺, IL-17⁺, IL-1β⁺, and caspase-1⁺ cells was observed, but no correlation between Th17 and the inflammasome response with evolutionary disease pathology was reported. These data showed the participation of Th17 cells and the inflammasome in the inflammatory response of the skin lesions of LCL caused by L. (V.) panamensis infection. These results suggest a role in the control of tissue parasitism of IL-17 and the activation of the NLRP3 inflammasome dependent on IL-1β but cannot exclude their role in the development of disease pathology.

中文翻译：

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炎症小体和 Th17 细胞参与由巴拿马利什曼原虫 (Viannia) 引起的人类皮肤利什曼病皮肤病变

引起局部皮肤利什曼病（LCL）的利什曼原虫（Viannia）panamensis是在巴拿马一个地方病。这种情况会导致溃疡性皮肤病变，其特征是导致疾病病理的 Th1/Th2 混合免疫反应。然而，原位炎症过程的维持涉及其他因素，例如 Th17 和炎症小体反应。尽管这些过程与寄生虫消除有关，但它们在疾病病理学增加中的作用不容忽视。因此，在利什曼原虫感染中的作用仍不清楚。从这个意义上说，本研究旨在表征 LCL 患者皮肤病变中的 Th17 和炎症小体反应。L. ( V. ) panamensis帮助阐明这种疾病在巴拿马的发病机制。Th17细胞和炎性应答通过免疫组织化学（IHQ）在从患者46个的皮肤活组织检查评价与LCL引起L.（V.）panamensis。使用 CD3、CD4、RoR γ t、IL-17、IL-6、IL-23 和 TGF- β1抗体评估 Th17 免疫反应，并通过 IL-1 β评估炎性体反应、IL-18 和 caspase-1 抗体。Th17 和炎症小体反应的存在由皮肤病变中所有免疫标志物的阳性反应证明。观察到无鞭毛体的密度与 RoR γ t ⁺、IL-17 ⁺、IL-1 β ⁺和 caspase-1 ⁺细胞的密度呈负相关，但 Th17 与炎症小体反应与进化疾病病理学之间没有相关性已经报道。这些数据表明Th17细胞和炎性体参与了L. ( V. ) panamensis引起的LCL皮损的炎症反应。感染。这些结果表明在控制 IL-17 的组织寄生和依赖 IL-1 β的 NLRP3 炎症小体的激活中起作用，但不能排除它们在疾病病理学发展中的作用。