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

Laurissa OuaguiaTania Dufeu-DuchesneVincent LeroyThomas DecaensJean-Baptiste ReiserEleonora Sosa CuevasDavid DurantelJenny Valladeau-GuilemondNathalie Bendriss-VermareLaurence ChaperotCaroline Aspord

Published in: Clinical & translational immunology (2020)

HBV may exploit CLR pathways to hijack DC subsets and escape from immune control. Such advances bring insights into the mechanisms by which HBV subverts immunity and pave the way for developing innovative therapeutic strategies to restore an efficient immune control of the infection by manipulating the viral glycan-lectin axis.

Keyphrases

hepatitis b virus
liver failure
cell cycle
sars cov
low density lipoprotein
cell proliferation