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. 2021 May 24;12:673912. doi: 10.3389/fimmu.2021.673912

Figure 5.

Figure 5

AAV monocytes are deficient for CMTM6, blocking lysosomal function restores capacity to upregulate PD-L1. (A, B) Monocytes from either HC (E) or AAV patients (F) were stimulated with IFNγ for 24 hours in the presence or absence of the lysosomal inhibitor BafA1 (20nM). Monocytes not treated with BafA1 inhibitor were treated with the corresponding vehicle. (C) Representative histograms of CMTM6 protein expression in IFNγ-stimulated (24 hours) monocytes from HC and AAV patients. (D) Summarizing scatter dot plot showing results from 10 experiments. (E) Correlation of PD-L1 expression with CMTM6 in IFNγ-stimulated monocytes in HC and AAV patients (each group n=10). (F) Gene expression of CMTM6 in monocytes from HC and AAV patients after stimulation with IFNγ for 24 hours measured by RT-PCR, relative to housekeeping gene β-actin. Paired t-test (A), Wilcoxon test (B), unpaired t-test (D), Spearman correlation (E), and Mann-Whitney test (F) were applied. ***P<0.01; ***P<0.001. Bar graph shows mean ± SEM. AAV, ANCA-associated vasculitis; HC, healthy control donors; MFI, mean fluorescence intensity; PD-L1, Programmed death-ligand 1; CMTM6, CKLF-like MARVEL transmembrane domain containing 6; BafA1, Bafilomycin A1; ns, statistically not significant.