Figure 3.

Fat Depot-specific Roles of Adipocyte Stem Cells (ASCs) in the Regulation of Adipose Tissue Immunity. White adipose tissues consist of major two fat depots; visceral adipose tissue and subcutaneous adipose tissue. These two fat depots exhibit several differences in inflammatory responses, fibrosis, and adipogenesis. ASCs are major cell types comprising of adipose tissue, and they are largely divided into adipogenic and non-adipogenic clusters. In visceral adipose tissue, there are fibro-inflammatory ASCs (lin−Pdgfrβ+Ly6c+ cells or lin−Pdgfrα+Gp38+CD9+). The number of fibro-inflammatory ASCs increases in obesity and they secret pro-inflammatory cytokines (e.g., IL-6, Ccl2) and ECM components (e.g., Col1a1, Col3a1), promoting fibrosis. Moreover, it has been reported that IL-33 producing non-adipogenic ASCs (lin−Pdgfrα+PPARγ−) are involved in recruitment of Treg and ILC2 via IL-33 secretion, which suppresses inflammation in visceral adipose tissue. Recently, it was reported that, in subcutaneous adipose tissue, ASCs (CD31−CD34+Sca1+) suppress monocyte infiltration, which is potentially regulated by GABA signaling. However, the secretory factors that inhibit monocyte infiltration in subcutaneous adipose tissue have not been elucidated yet.