Fig. 6

Increased inflammatory response and decreased unfolded protein response in LPS-treated MDMi cells with TYROBP deletion. A-C Volcano plots of differentially expressed genes and (D-F) proteins in the monoallelic TYROBP deletion carrier MDMi cells compared to controls upon untreated (A, D), myelin-treated (B, E) and lipopolysaccharide (LPS)-treated (C, F) conditions., T^CV, n = 3–12; T^del, n = 3. (G) Pathway enrichment of genes (left panel) and proteins (right panel) differentially expressed in the monoallelic TYROBP deletion carrier MDMi cells compared to TYROBP common variant MDMi cells. H-I Heat maps showing the top up- and downregulated targets in the UPR and MYC pathways in the monoallelic (H) and biallelic (I) TYROBP deletion carriers compared to controls. J-K Inflammatory response was assessed by measuring interleukin-6 (IL-6), IL-1β, IL-10 (J), and tumor necrosis factor α (TNFα; K) levels in the conditioned media of T^CV, T^del, and NHD MDMi upon 24 h LPS treatment. Each data point indicates one individual, an average of 1–3 replicate wells. T^CV, n = 3–4; T^del, n = 3–4; NHD, n = 1–2. All data in J are shown as mean ± SD. Independent samples T-test, *: P < 0.05. T^CV, TYROBP common variant; T^del, monoallelic TYROBP deletion; NHD, Nasu-Hakola disease