Leishmaniasis is a neglected infectious disease with clinical presentations ranging from asymptomatic or mild symptoms to chronic infection and eventual death. The mechanisms of disease susceptibility and pathology have been extensively studied, but there are no steadfast rules regarding leishmaniasis. A Th1 response is usually associated with infection control, while a predominant Th2 response is detrimental to the patient. In this scenario, the enzymes arginase and inducible nitric oxide synthase represent two possible pathways of immune response. While the former contributes to parasite replication, the latter is crucial for its control. In the present review, we collected study results that associate arginase expression in patients and in experimental models with disease susceptibility/chronicity and show some proposed mechanisms that explain the role of arginase in maintaining Leishmania infection, including polyamine and thiol synthesis, tissue‐resident macrophage (TRM) proliferation and activation and T‐cell suppression and exhaustion.

中文翻译：

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精氨酸酶及其在利什曼原虫持久性中的机制。

利什曼病是一种被忽视的传染病，其临床表现从无症状或轻度症状到慢性感染和最终死亡。疾病易感性和病理机制已得到广泛研究，但关于利什曼病尚无坚定的规则。Th1反应通常与感染控制相关，而占主导的Th2反应对患者有害。在这种情况下，精氨酸酶和诱导型一氧化氮合酶代表了两种可能的免疫反应途径。前者有助于寄生虫复制，而后者对其控制至关重要。在目前的评论中，利什曼原虫感染，包括多胺和巯基合成，组织驻留巨噬细胞（TRM）的增殖和活化以及T细胞的抑制和衰竭。