The finding that strong adhesion by regulatory T cells induces dendritic cell cytoskeletal polarization and contact-dependent lethargy is reported by Dr. Yan Shi and colleagues on the Journal of Experimental Medicine in January, 2017.

Dendritic cells are targeted by regulatory T (Treg) cells, in a manner that operates as an indirect mode of T cell suppression. In this study, using a combination of single-cell force spectroscopy and structured illumination microscopy, Dr. Shi and colleagues analyzed individual Treg cell-DC interaction events and show that T reg cells exhibit strong intrinsic adhesiveness to DCs. This increased DC adhesion reduces the ability of contacted DCs to engage other antigen-specific cells. They show that this unusually strong LFA-1-dependent adhesiveness of Treg cells is caused in part by their low calpain activities, which normally release integrin-cytoskeleton linkage, and thereby reduce adhesion. Super resolution imaging reveals that such Treg cell adhesion causes sequestration of Fascin-1, an actin-bundling protein essential for immunological synapse formation, and skews Fascin-1-dependent actin polarization in DCs toward the Treg cell adhesion zone. Although it is reversible upon Treg cell disengagement, this sequestration of essential cytoskeletal components causes a lethargic state of DCs, leading to reduced T cell priming. The results reveal a dynamic cytoskeletal component underlying T reg cell-mediated DC suppression in a contact-dependent manner.

The original paper could be found from the link: http://jem.rupress.org/content/214/2/327