Fig. 5From: Mir-155 is overexpressed in systemic sclerosis fibroblasts and is required for NLRP3 inflammasome-mediated collagen synthesis during fibrosismiR-155 and interleukin-1 (IL-1) provide a feed-forward mechanism during fibrosis. In fibroblasts, activation of the inflammasome drives miR-155 expression via IL-1 autocrine signaling that further enhances IL-1 transcription and leads to fibrosis. Blockade of the IL-1 receptor or the inflammasome abrogates this processBack to article page