A long noncoding RNA (lncRNA) called lincRNA-Cox2 is induced by Toll-like receptors (TLRs) and plays a key role in regulating immune responses. This study shows that lincRNA-Cox2 can both activate and repress immune genes. It interacts with heterogeneous nuclear ribonucleoproteins (hnRNP-A/B and A2/B1) to regulate gene expression. The lncRNA is induced in response to TLR signaling and is involved in the inflammatory response. It is expressed in macrophages and dendritic cells, and its expression is dependent on TLR signaling pathways, including MyD88 and NF-κB. The study also shows that lincRNA-Cox2 is not translated into a protein, as it lacks strong Kozak sequences. Functional studies demonstrate that lincRNA-Cox2 represses the expression of certain immune genes, such as Ccl5, while enhancing the expression of others, like Il6, in response to TLR stimulation. Additionally, lincRNA-Cox2 interacts with hnRNP-A/B and A2/B1 to regulate immune gene expression. These findings highlight the role of lncRNAs in immune regulation and suggest that they are important components of the innate immune response. The study also identifies hnRNP-A/B and A2/B1 as mediators of lincRNA-Cox2's transcriptional repressive functions. Overall, lincRNA-Cox2 is a critical regulator of immune gene expression and plays a broad role in the inflammatory response.A long noncoding RNA (lncRNA) called lincRNA-Cox2 is induced by Toll-like receptors (TLRs) and plays a key role in regulating immune responses. This study shows that lincRNA-Cox2 can both activate and repress immune genes. It interacts with heterogeneous nuclear ribonucleoproteins (hnRNP-A/B and A2/B1) to regulate gene expression. The lncRNA is induced in response to TLR signaling and is involved in the inflammatory response. It is expressed in macrophages and dendritic cells, and its expression is dependent on TLR signaling pathways, including MyD88 and NF-κB. The study also shows that lincRNA-Cox2 is not translated into a protein, as it lacks strong Kozak sequences. Functional studies demonstrate that lincRNA-Cox2 represses the expression of certain immune genes, such as Ccl5, while enhancing the expression of others, like Il6, in response to TLR stimulation. Additionally, lincRNA-Cox2 interacts with hnRNP-A/B and A2/B1 to regulate immune gene expression. These findings highlight the role of lncRNAs in immune regulation and suggest that they are important components of the innate immune response. The study also identifies hnRNP-A/B and A2/B1 as mediators of lincRNA-Cox2's transcriptional repressive functions. Overall, lincRNA-Cox2 is a critical regulator of immune gene expression and plays a broad role in the inflammatory response.