Hepatitis B virus exploits C‐type lectin receptors to hijack cDC1s, cDC2s and pDCs - Archive ouverte HAL Access content directly
Journal Articles Clinical and Translational Immunology Year : 2020

Hepatitis B virus exploits C‐type lectin receptors to hijack cDC1s, cDC2s and pDCs

Abstract

C-type lectin receptors (CLRs) are key receptors used by DCs to orchestrate responses to pathogens. During infections, the glycan-lectin interactions shape the virus-host interplay and viruses can subvert the function of CLRs to escape antiviral immunity. Recognition of virus/viral components and uptake by CLRs together with subsequent signalling cascades are crucial in initiating and shaping antiviral immunity, and decisive in the outcome of infection. Yet, the interaction of hepatitis B virus (HBV) with CLRs remains largely unknown. As HBV hijacks DC subsets and viral antigens harbour glycan motifs, we hypothesised that HBV may subvert DCs through CLR binding.
Fichier principal
Vignette du fichier
Ouaguia et al. CTI 2020.pdf (2.19 Mo) Télécharger le fichier
Origin : Publisher files allowed on an open archive

Dates and versions

hal-03183870 , version 1 (29-03-2021)

Identifiers

Cite

Laurissa Ouaguia, Tania Dufeu-Duchesne, Vincent Leroy, Thomas Decaens, Jean-Baptiste Reiser, et al.. Hepatitis B virus exploits C‐type lectin receptors to hijack cDC1s, cDC2s and pDCs. Clinical and Translational Immunology, 2020, 9 (12), pp.e1208. ⟨10.1002/cti2.1208⟩. ⟨hal-03183870⟩
77 View
92 Download

Altmetric

Share

Gmail Facebook Twitter LinkedIn More