TABLE 1.

Exosomal DAMPs and their impact on inflammation.

DAMPs in exosomes	Stimuli	Interacting pathway	Outcomes (production of pro-inflammatory molecules)
HMGB1	LPS (31), Pathogen (24), IL-1β (32), TNF-α (32)	TLR4 (31), Caspase-11/GSDMD (31), Autophagy deficiency (32), ER stress (33), NF-κB (24)	IL-1α (32), IL-1β (32), IL-6 (32), CCL2 (32), COX-2 (32)
HSPs	Heat shock (36), LPS (36), Pathogen (37), IL-1β (32), TNF-α (32)	Autophagy deficiency (32), ER stress (33), NF-κB (37)	TNF-α (37), IL-1α (32), IL-1β (32), IL-6 (32), CCL2 (32), COX-2 (32)
Histones	LPS (21)	TLR4 (21), ER stress (33)	TNF-α (21), IL-1β (21), IL-6 (21)
ATP	LPS (42)	P2Y11 (42)	TNF-α (42), IL-1β (42), IL-6 (42), IL-12 (42), M1 polarization (42)
exRNAs	LPS (51, 53)	TLRs (45), NLRs (45), RLRs (45), Apoptosis (46), NF-κB (52, 53), SOCS-1↓ (52, 53), SHIP1↓ (52)	MCP-1 (53), IL-1β (53), IL-6 (52, 53), TNF-α (52, 53), iNOS (53), MΦ proliferation (52), M1 polarization (53)

HMGB1, high mobility group box 1; TLR, Toll-like receptor; GSDMD, Gasdermin D; COX-2, cyclooxygenase-2; HSPs, heat shock proteins; ER, endoplasmic reticulum; ATP, adenosine triphosphate; exRNA, extracellular RNA; SOCS, suppressors of cytokine signaling; MCP-1, monocyte chemoattractant protein 1; SHIP1, Src homology 2 (SH2) domain containing inositol polyphosphate 5-phosphatase 1.