The blood vascular system of mammals is unique in nature; inhabited with a pool of tiny small cell fragments called platelets; attributed with the most important patrolling tasks to check integrity of the entire endothelial landscape. Their production is tightly coupled with hematopoietic system where everything starts from self renewable multipotent hematopoietic stem cells (HSCs) which eventually undergo dual step (megakaryopoiesis-thrombopoiesis) thrombocytes production. Several cytokines tune the fate of every progenitor cells during hematopoiesis through temporal activation of specific transcription factors. Though platelets generated through steady state hematopoiesis are involved in the regulation of vascular homeostasis, these cells can sense pathogens through its innate immune sensors and can mount crucial responses against the invading pathogen. For this, the primary aim of many infections including Leishmania is to induce thrombocytopenia within infected host. But the underlying mechanism of this induced thrombocytopenia in Leishmania infection has not been evaluated. Elucidation of these mechanisms will be fruitful to design new chemotherapeutic strategies.

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血小板生成在利什曼病中的作用

哺乳动物的血管系统在自然界中是独一无二的；居住着一池称为血小板的微小细胞碎片；归因于最重要的巡逻任务，以检查整个内皮景观的完整性。它们的生产与造血系统紧密结合，其中一切都从自我更新的多能造血干细胞 (HSC) 开始，最终经历双步骤（巨核细胞生成 - 血小板生成）血小板生成。几种细胞因子通过特定转录因子的时间激活来调节造血过程中每个祖细胞的命运。虽然通过稳态造血产生的血小板参与调节血管稳态，这些细胞可以通过其先天免疫传感器感知病原体，并对入侵的病原体产生关键反应。为此，包括利什曼原虫在内的许多感染的主要目的是在受感染的宿主内诱发血小板减少症。但尚未评估这种在利什曼原虫感染中诱发的血小板减少症的潜在机制。阐明这些机制将有助于设计新的化疗策略。