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. Author manuscript; available in PMC: 2023 Aug 9.
Published in final edited form as: Immunity. 2022 Aug 4;55(8):1386–1401.e10. doi: 10.1016/j.immuni.2022.06.022

Figure 2. Effect of deleterious mutations or ablation of DNTM3A or TET2 in bystander cells.

Figure 2.

(A) RT-qPCR (left) of IFNA1, IFNA4, and IFNA5 and protein secretion analysis by ELISA (right) of IFNα in MDM transfected with DNMT3A ASO or TET2 ASO (n ≥ 3 donors).

(B) Venn diagram and pathway analysis of genes differentially expressed in normal MDM incubated with conditioned media from macrophages transfected with DNMT3A ASO 1 or TET2 ASO 2(n = 4 donors).

(C) Representative examples of ISG expression in macrophages treated with conditioned media from macrophages transfected with DNMT3A ASO 1 or TET2 ASO 2.

(D) Analysis by RNA-seq of expression of ISG in macrophages incubated with conditioned media from macrophages transfected with DNMT3A ASO 1 or TET2 ASO 2 with and without IFNαR2 antibody (n = 2 donors).

(E) RT-qPCR of ISGs in MDM transfected with DNMT3A ASO or TET2 ASO with and without treatment with IFNα (n = 4 donors).

(F) Relative concentrations of IFNα in culture supernatant of macrophages differentiated from monocytes from two individuals with DNMT3A mutations or TET2 mutations compared to two individuals without detectable mutation (control 1 and control 2).

(G) RT-qPCR analysis of ISG expression in MDM treated with conditioned media of macrophages with DNMT3A or TET2 mutations versus conditioned media from control individuals. Mann-Whitney U test was used to calculate statistical significance in all panels except in (E) where Student’s t test was used. *p < 0.05; **p < 0.01. Also see Figures S1 and S3.