Pattern recognition receptors (PRRs) trigger adaptive inflammatory responses and as such are attractive targets for therapeutic manipulation of inflammation. In order to develop effective therapies however we need to understand the complexities of PRR signaling and clarify how individual PRRs contribute to an inflammatory response in a given cell type.

Data from our lab and others have shown that cross-talk occurs between different PRR family members that directs T cell responses to a particular stimuli. It is well-established that the cell surface toll-like receptor 2 (TLR2) provides a potent costimulatory signal for TCR-stimulated T cell activation. We have shown that signaling through the intracellular nucleotide-binding oligomerization domain-containing proteins 1 and 2 (Nod1 and Nod2) also provides important signals for T cell activation, and that when both Nod1 and Nod 2 are deleted stimulated T cells undergo activation-induced cell death.

This study found that TLR2 costimulation could bypass the defect induced by the simultaneous absence of Nods1 and 2 in both antibody- and antigen-stimulated T cells. Since blocking one set of PRR-mediated responses can be overcome by signaling through another PRR family member, then effective therapeutic immune blockade strategies will likely require a multi-pronged approach in order to be effective.

模式识别受体（PRR）触发适应性炎症反应，因此是炎症治疗操纵的有吸引力的靶标。然而，为了开发有效的治疗方法，我们需要了解 PRR 信号传导的复杂性，并阐明单个 PRR 如何促进特定细胞类型的炎症反应。

我们实验室和其他实验室的数据表明，不同 PRR 家族成员之间会发生串扰，引导 T 细胞对特定刺激做出反应。众所周知，细胞表面 Toll 样受体 2 (TLR2) 为 TCR 刺激的 T 细胞激活提供有效的共刺激信号。我们已经证明，通过含有蛋白质 1 和 2（Nod1 和 Nod2）的细胞内核苷酸结合寡聚化结构域的信号传导也为 T 细胞激活提供了重要信号，并且当 Nod1 和 Nod 2 都被删除时，刺激的 T 细胞会经历激活诱导的过程。细胞死亡。

这项研究发现，TLR2 共刺激可以绕过抗体和抗原刺激的 T 细胞中同时缺乏 Nods1 和 2 所引起的缺陷。由于阻断一组 PRR 介导的反应可以通过另一个 PRR 家族成员发出信号来克服，因此有效的治疗性免疫阻断策略可能需要多管齐下才能有效。