SARS-CoV-2 stimulation drives TLR7-dependent phenotypical modification in plasmacytoid Dendritic Cells.

Full article: https://doi.org/10.1371/journal.ppat.1009878

Purified plasmacytoid dendritic cells (pDC) were either left untreated (not stimulated, ns) or Mock-treated as negative controls, or stimulated for 24 hours with the TLR7/8 agonist R848 (5μM) as positive control, with SARS-CoV-2 (CoV2; MOI = 0.1) in presence or absence of a 30 minute pre-reatment with a specific TLR7/8 inhibitor (I-TLR7/8, 1μM).

(A) pDC were then stained with anti-BDCA4, PD-L1, CD80 and CD86 antibodies. The percentage (%) of pDC sub-populations was evaluated by flow cytometry in live/single BDCA4+ pDC; in particular P1-pDC (PD-L1+CD80-, in blue), P2-pDC (PD-L1+CD80+, in red) and P3-pDC (PD-L1-CD80+, in green).

(B) Surface expression of CD86, PD-L1 and CD80 was determined as mean fluorescence intensity (MFI) by flow cytometer analysis.

Regulation of innate immune responses elicited by SARS-CoV-2 VOCs.

Unpublished data, available soon for sharing

Different subsets of monocytes (A),

plasmacytoid dendritic cells (pDC) (B)

and conventional dendritic cells (cDC) (C) were analyzed in PBMC exposed to Omicron BA.1 and Omicron XBB.1.

Surface expression of the costimulatory marker CD86 was also determined as mean fluorescence intensity (MFI) in each cell subset (D-F).

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