Activation of the Innate Immune Checkpoint CLEC5A on Myeloid Cells in the Absence of Danger Signals Modulates Macrophages’ Function but Does Not Trigger the Adaptive T Cell Immune Response

Figure 6

CLEC5A agonistic Ab induces transcriptome changes in myeloid cell-specific genes. M0 MdM generated from same six donors as in Figure 5 were incubated for 6 h either with the α-CLEC5A Ab or with the isotype ctrl (10 μg/mL each) and then processed for the transcriptome analysis with NanoString nCounter. (a) Heat map of differentially expressed genes (preselected according to the quality criteria as described in the Materials and Methods) in M0 MdM exposed to the α-CLEC5A Ab (upper rows; each donor represented separately) as compared to the isotype ctrl (bottom rows). (b–e) Box plots showing expression of selected genes in M0 MdM upon treatment with α-CLEC5A Ab or isotype. Depicted are representative genes encoding soluble mediators (b), myeloid cell-specific surface receptors (c), selected cytokines from the IL-1 cytokine family with their functional partners (d), and a myeloid cell-specific transcription factor MAFB (e). Values represent mean and SD calculated from NanoString raw counts (each dot represents one individual donor). Shown is the summary result from two independent experiments with six donors; , , and .

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