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Updated: Feb 11, 2026

Purification of the Dendritic Filopodia-rich Fraction
Published on: May 2, 2019
Glycerol monolaurate induces filopodia formation by disrupting the association between LAT and SLP-76 microclusters
Michael S Zhang1, Phuong M Tran1, Alexander J Wolff1
1Department of Microbiology and Immunology, University of Iowa, Iowa City, IA 52242, USA.
Abstract:
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.
Insights
Glycerol monolaurate (GML) suppresses T cell function by disrupting actin cytoskeleton rearrangements. GML causes T cells to form filopodia instead of actin rings, impairing cell adhesion and migration.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Glycerol monolaurate (GML) is a monoglyceride known for its antimicrobial properties.
- GML suppresses T cell receptor (TCR)-induced signaling and effector functions.
- Actin cytoskeleton rearrangement is crucial for T cell interactions, migration, and effector functions.
Purpose of the Study:
- To investigate the effect of GML on actin cytoskeleton rearrangement following TCR activation in human T cells.
- To elucidate the molecular mechanisms by which GML interferes with TCR-induced actin dynamics.
Main Methods:
- Treated human T cells with GML and activated TCR signaling.
- Utilized microscopy techniques, including total internal reflection fluorescence microscopy (TIRFM), to visualize actin and protein microclusters.
- Analyzed the localization and colocalization of key proteins involved in actin polymerization and TCR signaling.
Main Results:
- GML-treated T cells exhibited reduced adherence and failed to form actin ring structures upon TCR activation.
- Instead of normal actin structures, GML-treated cells developed numerous filopodia.
- TIRFM revealed mislocalization of Arp2 microclusters in GML-treated cells, while SLP-76 and WASp microclusters showed altered colocalization patterns.
Conclusions:
- Glycerol monolaurate (GML) significantly alters actin cytoskeletal rearrangements in T cells.
- GML's T cell-suppressive effects are mediated, in part, by disrupting Arp2 microcluster organization and subsequent actin dynamics.
- These findings identify novel mechanisms for GML's immunomodulatory functions.
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