Dendritic cells (DCs) are at the forefront of the immune reaction.
When pathogens such as viruses invade, Toll-like receptors (TLR) and C-type lectin receptors (CLRs) expressed on DCs recognize the molecular structure peculiar to pathogens and trigger immune responses.
The CLR of DCs includes DCIR/CD367/CLEC4A, DECTIN1/CD369/CLEC7A, DECTIN2/CLEC6A, DNGR1/CD370/CLEC9A, MMR/CD206, DEC205/CD205, DC-SIGN/CD209, langerin/CD207, BDCA2/CD303/CLEC4C, etc.
The function of these lectins remain largely unknow, but for example,
DCIR binds to high mannose/fucose glycans and works inhibitory on the secretion of IL12 and TNFα, while DECTIN1 recognizes β-1,3-glucans and conversely promotes the secretion of these inflammatory cytokines.
A group of Univ. Grenoble Alpes discussed how the expression of various CLRs changes in chronic HBV based on experimental results performed using Flow cytometry.
https://onlinelibrary.wiley.com/doi/10.1002/cti2.1208
There are three subclasses of DC: CD1c/BDCA1 (cDC2s), CD141/BDCA3 (cDC1s), and plasmacytoid DCs (pDCs).
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Blood cDC2s: DECTIN1, MMR decreased,
Liver cDC2s: DCIR, MMR decreased,
Blood cDC1s: DECTIN1, CLEC9A decreased, Fcɣ Receptor increased slightly,
Liver cDC1s: DCIR, CLEC9A, Fcɣ receptor, MMR decreased, DECTIN1 increased slightly,
Blood pCDs: Little change,
Liver pCDs: DCIR increased, Fcε receptor increased slightly.
Such a change is happening.
Although the changes are very complex, it is worth noting that chronic HBV causes changes in the expression of CLRs in DCs.
Overall, CLR expression seems to be decreasing, which makes it easier for HBV to escape from immune system, right?