After traumatic injury, some cells function as detectors to sense injury and to modulate the local immune response toward a restitution phase by affecting the local cytokine milieu. Using intravital microscopy, we observed that patrolling invariant natural killer T (iNKT) cells were initially excluded from a site of hepatic injury but subsequently were strategically arrested first via self-antigens and then by cytokines, circumscribing the injured site at exactly the location where monocytes co-localized and hepatocytes proliferated. Activation of iNKT cells by self-antigens resulted in the production of interleukin-4 (IL-4) but not interferon-γ (IFN-γ). This promoted increased hepatocyte proliferation, monocyte transition (from Ly6C^hi to Ly6C^lo), and improved healing where IL-4 from iNKT cells was critical for these processes. Disruption of any of these mechanisms led to delayed wound healing. We have shown that self-antigen-driven iNKT cells function as sensors and orchestrators of the transformation from inflammation to tissue restitution for essential timely wound repair.

创伤性损伤后，一些细胞起着检测器的作用，通过影响局部细胞因子环境来感知损伤并向恢复阶段调节局部免疫应答。使用活体显微镜检查，我们观察到巡逻的恒定自然杀伤T（iNKT）细胞最初被排除在肝损伤部位之外，但随后首先通过自身抗原然后通过细胞因子被策略性地阻滞，将损伤部位限制在单核细胞的确切位置共定位，肝细胞增生。自身抗原激活iNKT细胞会产生白介素4（IL-4），但不会产生干扰素-γ（IFN-γ）。这促进了肝细胞增殖和单核细胞转化的增加（从Ly6C ^hi到Ly6C ^lo）和改善的愈合能力，其中来自iNKT细胞的IL-4对于这些过程至关重要。这些机制中的任何一种破坏都会导致伤口愈合延迟。我们已经表明，自身抗原驱动的iNKT细胞可作为从炎症到组织恢复的转化的传感器和协调器，以进行必要的及时伤口修复。