Cytokines are key mediators of immune responses to autoantigens, tumor antigens and foreign antigens including pathogens and transplant antigens. The cytokines are produced by a variety of immune and non-immune cells and are dynamically regulated. Remarkably, during toxic and septic shock syndromes, anaphylactic shock and in certain viral infections supra-physiologic levels of cytokine storms are produced culminating in multi-organ failure and death. However, Leishmania infection is a chronic parasitic infection with alternate outcomes- healing or non-healing. Leishmania invades macrophages and inflicts the complex of diseases called Leishmaniases. Depending on the species of Leishmania and the organs affected, the diseases are categorized into Cutaneous Leishmaniasis (CL), Muco-cutaneous Leishmaniasis (MCL) and Visceral Leishmaniasis (VL). After successful chemotherapy of VL, a dermal manifestation- termed post-kalazar dermal leishmaniasis (PKDL)- of the same infection occurs in some patients. The operational frameworks for different cytokines have been laid to discuss how these immune mediators control each of these forms of leishmaniases. One of these frameworks is the regulation of monocytopoiesis including the role of macrophages subsets and thrombopoiesis in leishmaniases. Macrophage metabolism is linked to different cytokines and is thereby associated with the manifestation of the resistance or susceptibility to Leishmania infection and of drug resistance. The chemokine-regulated immune cell movements present the landscape of infection and pathogenesis. T cells subsets- the IFN-γ-secreting Ly6C + T cells and the regulatory T cell subsets- provide the initial skewing of Th cell subset and regulation of effector Th subsets, respectively, eventually deciding the outcome of infection.

中文翻译：

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利什曼病中免疫和免疫发病机制中的细胞因子

细胞因子是对自身抗原、肿瘤抗原和外来抗原（包括病原体和移植抗原）的免疫反应的关键介质。细胞因子由多种免疫细胞和非免疫细胞产生，并受到动态调节。值得注意的是，在中毒性和感染性休克综合征、过敏性休克和某些病毒感染中，会产生超生理水平的细胞因子风暴，最终导致多器官衰竭和死亡。然而，利什曼原虫感染是一种慢性寄生虫感染，具有不同的结果——愈合或不愈合。利什曼原虫侵入巨噬细胞并造成称为利什曼病的复杂疾病。根据利什曼原虫的种类和受影响的器官，疾病分为皮肤利什曼病（CL）、皮肤黏膜利什曼病（MCL）和内脏利什曼病（VL）。在 VL 成功化疗后，一些患者会出现相同感染的皮肤表现——称为卡拉查后皮肤利什曼病 (PKDL)。已经建立了不同细胞因子的操作框架来讨论这些免疫介质如何控制这些形式的利什曼病。这些框架之一是调节单核细胞生成，包括巨噬细胞亚群和血小板生成在利什曼病中的作用。巨噬细胞代谢与不同的细胞因子有关，因此与对利什曼原虫感染的抗性或易感性和耐药性的表现有关。趋化因子调节的免疫细胞运动呈现感染和发病机制的景观。