Fig. 1. Developmental mechanisms and characteristics of adipose tissue macrophages (ATMs) in health and obesity. In lean states, resident ATMs primarily originate from yolk-sac progenitors and maintain their population through in situ proliferation. Over time, monocyte-derived ATMs infiltrate and replace these resident ATMs. Resident ATMs are dispersed across the tissue and are characterized by the anti-inflammatory cytokine interleukin 10 (IL-10). During obesity progression, resident ATMs can polarize into a pro-inflammatory phenotype marked by intracellular lipid accumulation. Increased recruitment and proliferation of pro-inflammatory lymphocyte antigen 6 family member C1 (Ly6C)+ monocytes, along with reduced cell egress, contribute to the elevation of ATM numbers. In obese states, ATMs tend to accumulate around dead adipocytes, forming crown-like structures (CLS) and secreting the pro-inflammatory cytokines Il-6, tumor necrosis factor α (TNF-α), and IL-1β. CCR2, C-C chemokine receptor type 2; CCL2, C-C motif chemokine ligand 2.
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