Glycerol monolaurate (GML) is a monoglyceride with potent antimicrobial properties that suppresses T cell receptor (TCR)–induced signaling and T cell effector function. Actin rearrangement is needed for the interaction of T cells with antigen-presenting cells and for migration to sites of infection. Because of the critical role actin rearrangement plays in T cell effector function, we analyzed the effect of GML on the rearrangement of the actin cytoskeleton after TCR activation. We found that GML-treated human T cells were less adherent than untreated T cells and did not form actin ring structures but instead developed numerous inappropriate actin-mediated filopodia. The formation of these filopodia was not due to disruption of TCR-proximal regulators of actin or microtubule polymerization. Instead, total internal reflection fluorescence microscopy demonstrated mislocalization of actin nucleation protein Arp2 microclusters, but not those containing the adaptor proteins SLP-76 and WASp, or the actin nucleation protein ARPC3, which are necessary for TCR-induced actin rearrangement. Additionally, SLP-76 microclusters colocalized with WASp and WAVE microclusters but not with LAT. Together, our data suggest that GML alters actin cytoskeletal rearrangements and identify diverse functions for GML as a T cell–suppressive agent.

甘油单月桂酸酯（GML）是一种具有强大抗菌特性的甘油单酸酯，可抑制T细胞受体（TCR）诱导的信号传导和T细胞效应子功能。T细胞与抗原呈递细胞的相互作用以及迁移到感染部位需要肌动蛋白重排。由于肌动蛋白重排在T细胞效应子功能中起关键作用，因此我们分析了GML对TCR激活后肌动蛋白细胞骨架重排的影响。我们发现，经GML处理的人T细胞比未处理的T细胞粘附少，并且不形成肌动蛋白环结构，而是发展出许多不适当的肌动蛋白介导的丝状伪足。这些丝状伪足的形成并不是由于肌动蛋白的TCR近端调节剂的破坏或微管聚合。反而，全内反射荧光显微镜显示肌动蛋白成核蛋白Arp2微簇的错误定位，但不包含包含衔接蛋白SLP-76和WASp或肌动蛋白成核蛋白ARPC3的微簇，TCR诱导的肌动蛋白重排是必需的。此外，SLP-76微簇与WASp和WAVE微簇共定位，但与LAT不在同一位置。总之，我们的数据表明GML可以改变肌动蛋白的细胞骨架重排，并可以识别GML作为T细胞抑制剂的多种功能。SLP-76微簇与WASp和WAVE微簇共定位，但不与LAT共定位。总之，我们的数据表明GML可以改变肌动蛋白的细胞骨架重排，并可以识别GML作为T细胞抑制剂的多种功能。SLP-76微簇与WASp和WAVE微簇共定位，但不与LAT共定位。总之，我们的数据表明GML可以改变肌动蛋白的细胞骨架重排，并可以识别GML作为T细胞抑制剂的多种功能。