Sensing of cell-associated HTLV by plasmacytoid dendritic cells is regulated by dense β-galactoside glycosylation.

Abstract:

:Human T Lymphotropic virus (HTLV) infection can persist in individuals resulting, at least in part, from viral escape of the innate immunity, including inhibition of type I interferon response in infected T-cells. Plasmacytoid dendritic cells (pDCs) are known to bypass viral escape by their robust type I interferon production. Here, we demonstrated that pDCs produce type I interferons upon physical cell contact with HTLV-infected cells, yet pDC activation inversely correlates with the ability of the HTLV-producing cells to transmit infection. We show that pDCs sense surface associated-HTLV present with glycan-rich structure referred to as biofilm-like structure, which thus represents a newly described viral structure triggering the antiviral response by pDCs. Consistently, heparan sulfate proteoglycans and especially the cell surface pattern of terminal β-galactoside glycosylation, modulate the transmission of the immunostimulatory RNA to pDCs. Altogether, our results uncover a function of virus-containing cell surface-associated glycosylated structures in the activation of innate immunity.

journal_name

PLoS Pathog

journal_title

PLoS pathogens

authors

Assil S,Futsch N,Décembre E,Alais S,Gessain A,Cosset FL,Mahieux R,Dreux M,Dutartre H

doi

10.1371/journal.ppat.1007589

subject

Has Abstract

pub_date

2019-02-28 00:00:00

pages

e1007589

issue

2

eissn

1553-7366

issn

1553-7374

pii

PPATHOGENS-D-18-01563

journal_volume

15

pub_type

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