Role of pro- and anti-inflammatory phenomena in the physiopathology of type 2 diabetes and obesity

Table 1 Summary of the key adipose tissue-infiltrating immune cells and secreted cytokines contributing to the pro-inflammatory status of adipose tissue in obesity and the anti-inflammatory status in lean individuals

Immune cell lineage	Main secreted cytokines	Biological activity	Lineage-inducing stimulus	Ref.
Pro-inflammatory AT in the obese condition
M1 macrophages	IL-1β	Recruited at the advanced stage of AT hypertrophy during obesity	Induced by saturated fatty acids	[4,5]
Th1	TNFα	Induce the recruitment of M1 macrophages to the AT		[65]
Th17	IL-17/IL-22	Induce the recruitment of M1 macrophages to the AT	Induced by purinergic signalling	[65,71,73]
Anti-inflammatory AT in lean individuals
M2 macrophages	IL-10, TGF-β Multiple chemokines (CCL17, 18, 22)	Secretion of multiple immunosuppressive cytokines and chemokines Phagocytosis of dead adipocytes	Induced by omega-3 polyunsaturated fatty acids Induced by IL-4 and IL-13	[16,20,21]
T-regs	IL-10	Promote polarization of M2 macrophages	Constitutively present in the AT of lean individuals	[13,16,47]
Th2	IL-4 and IL-13	Promote polarization of monocytes into M2 macrophages	IL-33	[43]
Eosinophils	IL-4	Promote “beiging” of adipose tissue.	Differentiation and activation dependent on GM-CSF, IL-3 and IL-5	[26]
		Promote UCP1 expression
ILC2’s	IL-5 and IL-13	IL-5 and IL-13 secretion by ILC2’s promotes eosinophils differentiation	IL-33 promotes the activation of ILC2’s	[41]

AT: Adipose tissue; ILC2s: Group 2 innate lymphoid cells; UCP1: Uncoupling protein 1; IL: Interleukin; TNF: Tumor necrosis factor; TGF: Transforming growth factor.