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Adenosine and Immune Imbalance in Visceral Leishmaniasis: The Possible Role of Ectonucleotidases

机译:内脏利什曼病中的腺苷和免疫失衡:外源核苷酸的可能作用。

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摘要

Visceral leishmaniasis (VL) is the most severe form of leishmaniasis and is responsible for most Leishmania-associated deaths. VL represents a serious public health problem that affects many countries. The immune response in leishmaniasis is very complex and is poorly understood. The Th1 versus Th2 paradigm does not appear to be so clear in visceral leishmaniasis, suggesting that other immunosuppressive or immune-evasion mechanisms contribute to the pathogenesis of VL. It has been demonstrated that generation of adenosine, a potent endogenous immunosuppressant, by extracellular enzymes capable to hydrolyze adenosine tri-nucleotide (ATP) at the site of infection, can lead to immune impairment and contribute to leishmaniasis progression. In this regard, this paper discusses the unique features in VL immunopathogenesis, including a possible role for ectonucleotidases in leishmaniasis.
机译:内脏利什曼病(VL)是最严重的利什曼病形式,是造成大多数与利什曼病相关的死亡的原因。 VL代表严重的公共卫生问题,影响许多国家。利什曼病的免疫反应非常复杂,人们对此知之甚少。在内脏利什曼病中,Th1与Th2的范式似乎不太清楚,这表明其他免疫抑制或免疫逃逸机制也有助于VL的发病。已经证明,通过在感染部位能够水解腺苷三核苷酸(ATP)的细胞外酶生成腺苷,一种有效的内源性免疫抑制剂,可导致免疫损伤并促进利什曼病的发展。在这方面,本文讨论了VL免疫发病机制的独特特征,包括胞外核苷酸酶在利什曼病中的可能作用。

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