Fig. 1: sMIC stimulation reprograms NK cells toward pro-inflammatory gene transcriptome.
Primary human NK cells enriched from PBMCs were stimulated with 100 ng/ml of recombinant sMICA in the absence or presence of sMIC-clearing monoclonal antibody B10G5 for 18 h. Total RNA was isolated for bulk RNA-sequencing analysis. a Heatmap representing the overall number of differentially expressed genes in human NK cells stimulated with sMICA, compared to the cells stimulated with sMICA in presence of B10G5. Primary mouse NK cells isolated from spleens of Rag−/− mice were stimulated with 100 ng/ml of recombinant sMICB in the absence or presence of B10G5 for 18 h. Total RNA was isolated for bulk RNA-sequencing analysis. b Heatmap representing the overall number of differentially expressed genes in mouse NK cells stimulated with sMICB, compared to the cells stimulated with sMICB in presence of B10G5. c Heatmap highlighting the key differentially expressed genes related to cytotoxicity and inflammatory response pathways in human NK cells upon stimulation with sMICA and sMICA+B10G5. d Heatmap highlighting the key differentially expressed genes related to cytotoxicity and inflammatory response pathways in mouse NK cells upon stimulation with sMICB and sMICB+B10G5. e Validation of representative genes associated with NK cell cytotoxicity and pro-inflammatory function (represented in (b) and (d)) by qRT-PCR. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001 (Student’s t test; two tailed).
