Table 1.

The potential mechanism of exosomal lncRNAs in the intestinal mucosal immune barrier.

Exosomal lncRNAs	Potential mechanism	References
H19	Antagonizes the negative regulatory factors of intestinal epithelial hyperplasia as an inflammatory lncRNA induced by IL22	[23]
	Participates in inflammatory diseases through VDR signaling	[26]
IFNG-AS1	Increases IFN-γ secretion of CD4+T cells	[27] [28] [29]
NEAT1	Participates in inflammatory response by regulating intestinal epithelial barrier and exocrine-mediated macrophage polarization	[31]
	Promotes IL-8 expression by relocating SFPQ	[32]
	Participates in TLR2-mediated expression of inflammatory cytokines	[34]
GAS5	Mediates intestinal mucosal by regulating the MMP expression	[44]
	Adjusts the LPS-induced inflammatory destruction by regulating KLF 2 expression and inhibiting the NF-κB pathway	[46]
HIF1-AS2	Inhibits NF-κB signaling pathway activation to protect the immune barrier	[48]
CDKN2B-AS1	Regulates inflammation of UC by sponging miR-195-5p and miR-16-5p and is negatively correlated with levels of inflammatory cytokines	[49] [50]
HOTAIR	Inhibits miR-218 and activates the NF-κB signaling pathway, resulting in the chemical resistance of CRC	[61]
	Acts as a scaffold to form PRC2 complex resulting in CRC development	[62]
CRNDE	Prevents Itch-mediated ubiquitination and degradation of RORγt to promote Th17 cell differentiation	[71]
MALAT1	Inhibits M2-type macrophage polarization and promotes M1-type macrophage polarization	[73]
	Acts as miR-155 sponge to reprogram DCs into a tolerant phenotype	[75]
RPPH1	Stimulates CRC cell metastasis by promoting exosome-mediated macrophage M2 polarization	[78]
MEG3	Inhibits CRC cell invasion and migration via regulating MMP-2, MMP-9, and TIMP-2	[80, 81]
	Inhibits LPS-induced macrophage apoptosis and secretion of inflammatory factors	[82]
HCG14	Alters NOD1 expression in intestinal cells	[87]
lnc-Smad3	Inhibits Treg cell polarization resulting in T cell-mediated colitis	[88]