Cutaneous leishmaniasis (CL) is a major public health problem worldwide and spreads to human via the bite of sand flies during blood meal. Following its inoculation, the promastigotes are immediately taken up by phagocytic cells and these leishmania-infected host cells produce proinflammatory cytokines that activate other immune cells and these infected host cells produce more cytokines and reactive nitrogen and oxygen species for efficient control of leishmania infection. Many experimental studies showed that resistance to infection with leishmania paraites is associated with the production of proinflammatory cytokines and activation of CD4⁺ Th1 response. On the other hand, vulnerability to this parasitic infection is correlated to production of T helper 2 cytokines that facilitate persistence of parasites and disease progression. In addition, some studies have also indicated that CD8⁺ T cells play a vital role in immune defense through cytokine production and their cytotoxic activity and excessive production of proinflammatory mediators promote amplified recruitment of cells. This could be correlated with excessive inflammatory reaction and ultimately resulted in tissue destruction and development of immunopathogenesis. Thus, there are contradictions regarding the role of immune responses in protection and immunopathogenesis of CL disease. Therefore, the aim of this paper was to review the role of host immune response in protection and its contribution to disease severity for CL infection. In order to obtain more meaningful data regarding the nature of immune response to leishmania, further in-depth studies focused on immune modulation should be conducted to develop better therapeutic strategies.

中文翻译：

---

宿主免疫反应在皮肤利什曼病感染过程中的保护和免疫发病机制中的作用综述。

皮肤利什曼病（CL）是世界范围内的主要公共卫生问题，在进餐期间会通过of蝇叮咬传播到人类。接种后，前鞭毛体立即被吞噬细胞吸收，这些感染了利什曼原虫的宿主细胞会产生促炎细胞因子，从而激活其他免疫细胞，而这些感染的宿主细胞会产生更多的细胞因子以及活性氮和氧，以有效控制利什曼原虫感染。许多实验研究表明，抵抗利什曼原虫寄生虫感染与促炎细胞因子的产生和CD4 ^+的激活有关Th1反应。另一方面，这种寄生虫感染的脆弱性与有助于寄生虫的持久性和疾病进展的T辅助细胞2细胞因子的产生有关。此外，一些研究还表明CD8 ⁺T细胞通过细胞因子的产生在免疫防御中起着至关重要的作用，它们的细胞毒活性以及促炎性介质的过量产生促进了细胞的募集。这可能与过度的炎症反应有关，并最终导致组织破坏和免疫发病机制的发展。因此，关于免疫应答在CL疾病的保护和免疫发病机理中的作用存在矛盾。因此，本文的目的是综述宿主免疫应答在保护中的作用及其对CL感染疾病严重性的影响。为了获得有关针对利什曼原虫的免疫反应的性质的更有意义的数据，应进行针对免疫调节的进一步深入研究，以开发更好的治疗策略。