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

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.

Mots clés

immune subversion hepatitis B virus HBsAg glycans DC subsets C‐type lectin receptor C-type lectin receptor

Domaines

Biologie structurale [q-bio.BM]

Fichier principal

Ouaguia et al. CTI 2020.pdf (2.19 Mo)

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https://hal.univ-grenoble-alpes.fr/hal-03183870

Soumis le : lundi 29 mars 2021-08:18:56

Dernière modification le : mardi 25 juillet 2023-16:35:22

Archivage à long terme le : mercredi 30 juin 2021-18:10:35

Dates et versions

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

Identifiants

HAL Id : hal-03183870 , version 1
DOI : 10.1002/cti2.1208
PUBMED : 33312564
PUBMEDCENTRAL : PMC7723857

Citer

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⟩

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