Table 2.

Current studies of exosomes from nonimmune cells on immune responses in T2DM.

Source	Contents	Functions	Expression in diabetic status	Immune responses	Experimental model	References
Pancreatic β-cells	miRNA-29	Promoting the recruitment and activation of circulating monocytes and macrophages and, hence, inflammation, via miR-29 exosomes in a TRAF3-dependent manner	Upregulate	Proinflammatory	HFD mice	Sun et al. [43]
Adipose tissue	Sonic hedgehog (Shh)	Inducing proinflammatory or M1 polarization of bone marrow-derived macrophages (BMDM) and RAW 264.7 macrophages	Upregulate	Proinflammatory	3T3-L1 adipocytes	Song et al. [46]
Adipose tissue	Adipose tissue exosome-like vesicles	Targeting the macrophages to the liver and adipose tissues, secrete TNF-α and IL-6 via the TLR4/TRIF pathway	Upregulate	Proinflammatory	HFD mice	Deng et al. [47]
Adipose tissue	MicroRNA-34a	Targeting the transcription factor KLF4	Upregulate	Proinflammatory	HFD mice	Pan et al. [10]
Adipose-derived stem cells (ADSCs)	ADSC-derived exosomes	Inducing high levels of M2-related Arg-1 and IL-10 and inhibiting macrophage inflammatory responses stimulated by LPS plus IFN-γ	Upregulate	Anti-inflammatory	HFD mice	Zhao et al. [52]

The exosomes miRNA-29, Shh, adipose tissue ELVs, and microRNA-34a are derived from nonimmune cells and play a role in promoting inflammation in T2DM, whereas ADSC-derived exosomes show anti-inflammatory effect.