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首页> 外文期刊>Infection and immunity >CD40-CD40 Ligand Costimulation Is Not Required for Initiation and Maintenance of a Th1-Type Response to Leishmania major Infection
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CD40-CD40 Ligand Costimulation Is Not Required for Initiation and Maintenance of a Th1-Type Response to Leishmania major Infection

机译：对于利什曼原虫主要感染的Th1型应答的启动和维持，不需要CD40-CD40配体共刺激。

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Although previous studies demonstrated a requirement for CD40-CD40 ligand (CD40L) interaction in the development of resistance to Leishmania infection, we recently showed that mice lacking the gene for CD40L (CD40L?/? mice) can control Leishmania major infection when they are infected with reduced numbers of parasites. In this study, we examine the cytokine pattern in healing versus nonhealing CD40L?/? mice and investigated whether CD40 activation is required for resistance to reinfection. We observed that CD4+ cells in healed CD40L?/? mice produce high levels of gamma interferon compared to cells from nonhealing, high-dose-inoculated mice. In addition, we observed a higher frequency of interleukin-12 (IL-12)- producing cells and a reduced number of IL-4-producing cells in mice infected with reduced numbers of parasites. Importantly, we found that healed CD40L?/? mice are highly resistant to reinfection with a large parasite inoculum. In addition, by comparing the cytokine patterns at an early and late stage of infection in nonhealing CD40L?/? mice, we demonstrated that nonhealing CD40L?/? mice produce a weak Th1-type response during the early stage of infection, but this response wanes as a Th2-type response emerges during late stages of infection. Anti-IL-4 antibody treatment, starting either at the beginning of infection or at week 4 postinfection enabled CD40L?/? mice to control a high-dose infection. Together, these results show that CD40-CD40L interaction, although important for IL-12 production in high-dose infections, is not required for either the development or maintenance of resistance in mice infected with reduced numbers of parasites.
机译：尽管先前的研究表明在对利什曼原虫感染的抗性发展中需要CD40-CD40配体（CD40L）相互作用，但我们最近发现小鼠缺乏CD40L（CD40L ？/？< / sup>小鼠）在感染了数量减少的寄生虫后即可控制 Leishmania major 感染。在这项研究中，我们检查了与未治愈的CD40L ？/？小鼠相比，愈合中的细胞因子模式，并研究了CD40激活是否需要抗感染性。我们观察到，与未治愈的高剂量接种小鼠相比，治愈的CD40L α/β小鼠中的CD4 + 细胞产生高水平的γ干扰素。此外，在感染了减少数量的寄生虫的小鼠中，我们观察到产生白介素12（IL-12）的细胞频率更高，产生IL-4的细胞数量减少。重要的是，我们发现已治愈的CD40L ？/？小鼠对大型寄生虫接种物的再感染具有高度抗性。此外，通过比较未治愈的CD40L ？/？小鼠感染早期和晚期的细胞因子模式，我们证明了未治愈的CD40L ？/？小鼠产生的免疫力较弱。在感染的早期阶段出现Th1型应答，但随着在感染的后期出现Th2型应答而减弱。从感染开始或感染后第4周开始进行抗IL-4抗体治疗，可使CD40L ？/？小鼠控制高剂量感染。总之，这些结果表明，CD40-CD40L相互作用尽管对于高剂量感染中IL-12的产生很重要，但对于感染或减少寄生虫数量的小鼠的耐药性的形成或维持，并不需要。

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