Plasmodium falciparum infection and malaria remain a risk for millions of children and pregnant women. Here, we seek to integrate knowledge of mouse and human T helper cell (Th) responses to blood-stage Plasmodium infection to understand their contribution to protection and pathology. Although there is no complete Th subset differentiation, the adaptive response occurs in two phases in non-lethal rodent Plasmodium infection, coordinated by Th cells. In short, cellular immune responses limit the peak of parasitemia during the first phase; in the second phase, humoral immunity from T cell-dependent germinal centers is critical for complete clearance of rapidly changing parasite. A strong IFN-γ response kills parasite, but an excess of TNF compared with regulatory cytokines (IL-10, TGF-β) can cause immunopathology. This common pathway for pathology is associated with anemia, cerebral malaria, and placental malaria. These two phases can be used to both understand how the host responds to rapidly growing parasite and how it attempts to control immunopathology and variation. This dual nature of T cell immunity to Plasmodium is discussed, with particular reference to the protective nature of the continuous generation of effector T cells, and the unique contribution of effector memory T cells.

中文翻译：

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利用 CD4 T 细胞对血期鼠疟疾的两个阶段反应来了解恶性疟原虫感染中全身免疫和胎盘病理的调节。


恶性疟原虫感染和疟疾仍然是数百万儿童和孕妇面临的风险。在这里，我们寻求整合小鼠和人类 T 辅助细胞 (Th) 对血液阶段疟原虫感染的反应知识，以了解它们对保护和病理学的贡献。尽管不存在完整的 Th 亚群分化，但在非致命性啮齿动物疟原虫感染中，适应性反应发生在两个阶段，由 Th 细胞协调。简而言之，细胞免疫反应限制了第一阶段寄生虫血症的峰值；在第二阶段，T细胞依赖性生发中心的体液免疫对于彻底清除快速变化的寄生虫至关重要。强烈的 IFN-γ 反应可杀死寄生虫，但与调节性细胞因子（IL-10、TGF-β）相比，过量的 TNF 会导致免疫病理学。这种常见的病理途径与贫血、脑型疟疾和胎盘型疟疾有关。这两个阶段可用于了解宿主如何响应快速生长的寄生虫以及它如何尝试控制免疫病理学和变异。讨论了 T 细胞对疟原虫免疫的双重性质，特别是效应 T 细胞的连续生成的保护性质，以及效应记忆 T 细胞的独特贡献。