Extended Data Fig. 1: CD38 expression in human M1 macrophages and analysis of the de novo NAD pathway in BMDMs.
From: Senescent cells promote tissue NAD+ decline during ageing via the activation of CD38+ macrophages
a, mRNA levels of CD38 in human peripheral blood monocytes (PBMC)-derived macrophages treated with recombinant human IL-4 (M2) or LPS (M1) for 18 hours. Representative data from one of three patient samples. (n = 4 independent biological experiments) b, Immunofluorescence of human PBMC derived macrophages stimulated as described above using an anti-human CD38 antibody (Green) and nuclei with DAPI (Blue). Scale bars represents 10μm. Analyzed in PBMCs derived from one patient. c, NADase activity in human PBMC-derived macrophages treated with recombinant human IL-4 (M2) or LPS (M1) for 18 hours. Shown is the mean of two separate experiments from different donors with 2 replicates each. d, Schematic of the de novo NAD synthesis pathway. e, mRNA levels of de novo NAD synthesis pathway enzymes. f, Quantification of tryptophan metabolites measured by LC-MS in M0, M2 and M1 mouse BMDMs activated for 24 hours. ND=not detected. Data shows the mean ± SEM n=3 independent experiments except in A and B. Statistical significance indicated as *P<0.05, **P<0.01, and ***P<0.001; two-sided Student’s t-test.
