The study investigates the induction of microRNA-155 (miR-155) in primary murine macrophages in response to various inflammatory stimuli. Using microarray technology, miR-155 was identified as the only miRNA significantly up-regulated by both polyribosinic:polyribocytidylic acid (poly(I:C)) and interferon-β (IFN-β). Additionally, miR-155 was induced by several Toll-like receptor (TLR) ligands through MyD88- or TRIF-dependent pathways, and by IFNs through TNF-α autocrine signaling. Pharmacological inhibition of the JNK kinase blocked miR-155 induction by poly(I:C) and TNF-α, suggesting that the JNK pathway is involved in miR-155 induction. These findings highlight miR-155 as a common target of a broad range of inflammatory mediators and suggest a potential link between inflammation and cancer, given miR-155's oncogenic properties.The study investigates the induction of microRNA-155 (miR-155) in primary murine macrophages in response to various inflammatory stimuli. Using microarray technology, miR-155 was identified as the only miRNA significantly up-regulated by both polyribosinic:polyribocytidylic acid (poly(I:C)) and interferon-β (IFN-β). Additionally, miR-155 was induced by several Toll-like receptor (TLR) ligands through MyD88- or TRIF-dependent pathways, and by IFNs through TNF-α autocrine signaling. Pharmacological inhibition of the JNK kinase blocked miR-155 induction by poly(I:C) and TNF-α, suggesting that the JNK pathway is involved in miR-155 induction. These findings highlight miR-155 as a common target of a broad range of inflammatory mediators and suggest a potential link between inflammation and cancer, given miR-155's oncogenic properties.