Dendritic cells play an important role in the development of immune responses in malaria, but the contribution of plasmacytoid dendritic cells (pDC) to CD4 T cell activation and immunopathology is unknown. We have investigated pDC in a Plasmodium chabaudi infection in mice. During infection, pDC increased in number and transiently up-regulated expression of Major Histocompatibility Complex class II and co-stimulatory molecules. However, in contrast to classical CD11c(high) DC, pDC could not phagocytose parasites or process parasite proteins, to activate CD4 T cells. Activation of naïve pDC, but not CD11c(high) DC, by infected red blood cells induced IFN alpha in vitro, which was dependent on the Toll-like receptor, TLR9. However, inactivation of TLR9 in knock-out mice had no effect on a P. chabaudi infection suggesting that TLR9 was not crucial for parasite elimination or pathology. Neither pDC nor IFN alpha beta were essential for parasite clearance as mice depleted of pDC or IFN alpha beta Receptor-knock-out mice could control infection. However, these mice lost significantly more weight than untreated or wild-type mice. We conclude that classical DC are the major antigen-presenting cells for CD4 T cells in this infection, but that pDC and IFN alpha beta may play minor roles in controlling the magnitude of acute stage pathology.

中文翻译：

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经典的 CD11c+ 树突细胞，而不是浆细胞样树突细胞，诱导 T 细胞对沙包疟原虫疟疾的反应。

树突状细胞在疟疾免疫反应的发展中发挥重要作用，但浆细胞样树突状细胞 (pDC) 对 CD4 T 细胞活化和免疫病理学的贡献尚不清楚。我们已经在小鼠的沙包疟原虫感染中研究了 pDC。在感染期间，pDC 的数量增加，主要组织相容性复合体 II 类和共刺激分子的表达瞬时上调。然而，与经典的 CD11c(high) DC 相比，pDC 不能吞噬寄生虫或处理寄生虫蛋白，以激活 CD4 T 细胞。受感染的红细胞在体外激活初始 pDC，而不是 CD11c(high) DC，诱导 IFN α，这依赖于 Toll 样受体 TLR9。然而，敲除小鼠中 TLR9 的失活对 P. chabaudi 感染表明 TLR9 对寄生虫消除或病理学并不重要。pDC 和 IFN α β 都不是寄生虫清除所必需的，因为耗尽 pDC 或 IFN α β 受体敲除小鼠的小鼠可以控制感染。然而，这些小鼠比未治疗或野生型小鼠的体重明显减轻。我们得出结论，经典 DC 是这种感染中 CD4 T 细胞的主要抗原呈递细胞，但 pDC 和 IFN α β 在控制急性期病理的大小方面可能起次要作用。