GSE134082
Transcriptomic analysis of Clec12A-deficient BMDCs stimulated with RIG-I agonist
Innate  immune receptors rely on the detection of diverse immunological cues and intensive crosstalk to generate context-dependent responses. The inhibitory C-type lectin receptor Clec12A has been shown to sense dead cells and danger-associated molecule uric acid crystal, and to subsequently limit inflammation. However, whether Clec12A plays additional roles in innate immunity has not yet been determined. Here we demonstrate that the activation of Clec12A enhances the induction of type I interferon (IFN-I) response. Through integrating data from RNA-seq, gene set enrichment analysis, and biochemical studies, we show that Clec12A is required for optimal transcription of interferon-stimulated genes in response to pattern recognition receptors (e.g. RIG-I) activation. Overall design: BMDCs generated from 4 WT and 4 Clec12A deficient mice were untreated, or stimualted with 3pRNA alone, or costimulated with 3pRNA and MSU crystals. The RNA were extracted from those cells and  analysed by RNA-sequencing.