| lincRNA-COX2 |
First identified in LPS-stimulated mouse CD11C+ BMDCs, and regulates inflammatory gene expression by interacting with hnRNP-A/B and hnRNP-A2/B1, and its expression was induced by TLR ligands in a MyD88- and NF-κB-dependent manner |
32,36,37
|
| PACER |
Activates COX-2 expression by occluding p50-p50 complexes in primary human mammary epithelial cells and PMA-stimulated human monocyte–macrophage cells |
38 |
| Lethe |
Binds to the RelA homodimer to block RelA-DNA binding and attenuates the NF-κB-dependent inflammatory response in MEFs following stimulation of TNFα, IL-1β, and dexamethasone |
17 |
| THRIL (linc1992) |
Interacts with hnRNPL to form a transcriptional activating complex and then binds to the TNF-α promoter to regulate TNF-α expression through a negative feedback mechanism with the induction upon TLR1/2 signaling in THP1-derived macrophages |
39 |
| NEAT1 |
Binds to SFPQ, so that SFPQ is translocated from the IL-8 promoter region to the paraspeckles, which in turn results in the activation of IL-8 in the TLR3-p38 signaling pathway |
40,41
|
| lncRNA-CMPK2 |
Has a negative regulatory role in the modulation of the IFN response. Consistently, lncRNA-CMPK2 is strongly upregulated in a subset of HCV-infected human livers |
44 |
| lncISG15 and lncBST2 |
Induced by influenza and VSV mutants that are unable to block the IFN response, and their expression increases with HCV infection and in the liver of infected patients |
45 |
| IL-1β-eRNA and IL-1β-RBT46 |
Is nuclear-localized, NF-κB-regulated, and favors LPS-induced messenger RNA transcription and the release of the pro-inflammatory mediators, IL-1β and CXCL8 |
46,47
|
| NKILA |
Binds to the NF-κB/IkB complex and represses NF-κB signaling and cancer-associated inflammation with induction by LPS, TNF-α, and IL-1β |
43 |
| Multiple |
15 elncRNAs and 12 plncRNAs were identified in LPS-induced BMDMs according to chromatin signatures defined by relative levels of H3K4me1 and H3K4me3 surrounding the transcription start site |
42 |
| Multiple |
7419 lincRNAs were analyzed in CD14+ monocytes that were isolated from RA patients treated with anti-IL-6R or anti-TNF-α, and the regulation of lincRNA transcription was highly specific for distinct cytokines |
48 |
