Table 2 Studies of correlations between tsRNAs and inflammatory mediators

tDR-1: 23-fMet-CAT-1

reduces LPS-induced and OMV-induced IL-8 secretion by cultured primary human airway epithelial cells

[7]

tDR-1:30-fMet-CAT-1

decreases LPS- or OMV-induced IL-8 secretion in AGS cells

[8]

tDR-1:30-Gly-CCC-2

promotes RSV replication and the expression of RSV-induced IL-6, IL-8, MIP-1β and CCL5 in airway epithelial cells, enhancing the inflammatory response

[9]

tDR-1:30-Lys-CTT-2-M2

tDR-56:71-Ala-CGC-1-M4

suppresses the expression of inflammatory cytokines IL-1β and TNF-α and inhibits apoptosis of NP cells

[33]

tDR-60:76-Cys-GCA-2-M7

inhibits JAK3 expression via AGO/RISC formation in chondrocytes, thereby suppressing downstream target cytokine IL-6 expression and preventing pro-inflammatory signaling, to restore cellular homeostasis

[34]

tDR-1:34-Ala-CGC-1-M3-D22GC-A25G-U26C

activates p65 and enhances IL-8 secretion in response to arsenite administration

[37]

tDR-1:19-Arg-ACG-1-M2

increases production of pro-inflammatory cytokines IL-1β and IL-18

[35]

tDR-1:32-Gly-GCC-1

upregulated in triple-negative breast cancer, mainly involved in the maintenance of stem cell population and cellular response to IL-6 secretion

[38]

tDR-1:32-Gly-GCC-1-C31A

tRF-36

promotes inflammatory factors TNF-α, IL-6, and IL-1β levels in an AP cell model generated from MCP-83 cells

[39]

tRF-47/tRF-47-58ZZJQJYSWRYVMMV5BO

reduces the release of IL-6, TNF-α, IL-10, IL-17 and IL-4 in a model of nonalcoholic steatohepatitis and improves the inflammatory response

[36]