Figure 1.

Adipose tissue inflammation in obesity. In the normal state, resident ATMs mostly show an M2-like polarized phenotype. Factors released from Tregs and eosinophils support ATMs to maintain this anti-inflammatory state. In obesity, increased adipocyte chemokine production induces increased blood monocyte recruitment, as well as ATM proliferation. The majority of monocyte-derived ATMs express CD11c and/or CD9 and the M1-like polarized phenotype. The decreased number of eosinophils and Tregs and the increased number of neutrophils, ILC1, CD8+ T cells, Th1 cells, and B2 cells enhance M1-like ATM polarization and adipose tissue inflammation.