lncRNAs Regulate Innate Immune Responses and Their Roles in Macrophage Polarization

Table 1

lncRNAs regulate the innate immune responses.

lncRNAs	Description of evidence	References
lincRNA-Cox2	lincRNA-Cox2 regulates the expression of inflammatory genes by binding with hnRNP-A/B and A2/B1. It also can interact with SWI/SNF complex in macrophages, to create lincRNA-Cox2/SWI/SNF complex, subsequently mediating SWI/SNF-associated chromatin remodeling and transcriptional activation of the late-primary inflammatory response genes. lincRNA-Cox2 represses the transcription of IL-12b in response to TNF-α stimulation.	[21–24]
PACER	PACER interacts with the repressive NF-κB subunit p50, enables it divorced from the COX-2 promoter, and favors the recruitment of the p300 histone acetyltransferase and RNA polymerase II (RNAPII) preinitiation complexes in the promoter region of Cox2 to promote COX-2 transcription.	[25]
Lethe	Lethe binds to the active NF-κB subunit p65 (RelA) and prevents it from binding to the promoters of target genes, thus reducing the production of inflammatory proteins, such as IL-6, IL-8, and superoxide dismutase 2 (SOD2).	[26]
THRIL	THRIL interacts with hnRNPL to establish a functional THRIL-hnRNPL complex, consequently regulating TNF-α transcription by binding to its promoter.	[28]
NEAT1	NEAT1 binds to SFPQ, relocating it from the IL-8 promoter to the paraspeckles and resulting in the activation of IL-8 transcription; knockdown of NEAT1 can enhance virus production by increasing nucleus-to-cytoplasm export of HIV-1 mRNA.	[29–31]
AS-IL1α	AS-IL1α favors the recruitment of RNAPII to the IL-1α promoter, thus controlling the transcriptional activation of IL-1α.	[32]
Lnc-IL7R	Lnc-IL7R regulates trimethylation of histone H3 at lysine 27 (H3K27me3) and increases its level at the promoters of E-selectin and VCAM-1, suppressing the expression of the two genes.	[33]
Lnc-DC	Lnc-DC promotes phosphorylation and activation of STAT3, a transcription essential for DC differentiation, by blocking its dephosphorylation by SHP1.	[35]
HOTAIRM1	HOTAIRM1 regulates RA-induced expression of HOXA1 and HOXA4 during the RA-induced granulocyte differentiation of NB4 cells and promotes induction of CD11b and CD18 expression, two hallmarks for granulocyte differentiation.	[40]
IL-1β-eRNA and IL1β-RBT46	IL-1β-eRNA or IL1β-RBT46 regulates LPS-induced production of the proinflammatory factors, such as IL-1β and CXCL8.	[41]
FIRRE	FIRRE can positively regulate the expression of several inflammatory genes at the posttranscriptional level through its interaction with hnRNPU.	[44]