Complement and regulatory T cells:The effect of complement on regulatory T cell responses in a mouse retrovirus model.

慢性病毒感染的建立可能是调节性T细胞(Treg)诱导和扩增的结果。越来越多的证据表明，树突状细胞(DC)参与了Treg的扩张，但DC-Treg相互作用的机制仍不清楚。使用Friend病毒模型，一种慢性逆转录病毒感染的小鼠模型，我们发现在缺乏补体成分C3的敲除小鼠中，Treg的扩张受损。因此，我们想要阐明补体在逆转录病毒感染期间诱导Treg反应中的作用。为此，我们将研究逆转录病毒颗粒的补体调理作用在多大程度上通过抗原提呈树突状细胞影响Treg的扩张。我们将进一步测试干扰补体激活和调理是否会影响Treg的扩张。这些研究将扩大我们对Tregs和DC相互作用的理解，这可能对从治疗上克服慢性病毒感染中的免疫逃避具有重要意义。

Establishment of chronic viral infections might be a consequence of the induction and the expansion of regulatory T cells (Tregs). Growing evidence suggests that dendritic cells (DC) are involved in the expansion of Tregs but the mechanisms of DC-Treg interaction are still elusive. Using the Friend virus model, a mouse model for chronic retroviral infections, we found an impaired Treg expansion in knock-out mice deficient for the complement component C3. Thus, we want to elucidate the role of complement in the induction of Treg responses during retroviral infections. To this end, we will study to which extent complement-opsonization of retroviral particles influences the expansion of Tregs via antigen-presenting DCs. We will further test if interfering with complement activation and opsonization affects the expansion of Tregs. The studies will extend our understanding about the interaction of Tregs and DCs, which might potentially be important to therapeutically overcome immune evasion in chronic viral infections.