Fig. 1

Network and physiological functions of resident immune cells in lean visceral adipose tissue. In the absence of metabolic or inflammatory stress resident immune cells interact among themselves and with adipocytes and stromal cells to maintain proper tissue functions. There are no signature cytokines defining the maintenance state of resident immune cells. Rather, the concept of a buffered system applies, without polarization towards a Th1/M1- or Th2/M2-like pattern or towards another biased state of immune reactivity. Cytokines, chemokines, acute phase proteins, and other immune mediators are released in small amounts mostly from resident immune cells but also from mesenchymal stromal cells and adipocytes. Several macrophage subtypes promote matrix remodeling and angiogenesis, phagocytose dead cell and lipid aggregates, and promote adipocyte thermogenesis. ILC2 also supports adipocyte thermogenesis and stimulates physiological eosinophil functions. Regulatory T cells promote tissue repair and interact with macrophages and other immune cell types to maintain a non-inflammatory state. Low-level secretion of immune mediators by macrophages, dendritic cells, and other immune cell types such as ILC2s, iNKTs, Th2 cells, γδT cells, B-1b cells, and eosinophils helps to prevent immune cell activation. For better readability, only a few key intercellular signals are included in the scheme. ATM, adipose tissue macrophage; DC, dendritic cell; IL, interleukin; ILC, innate lymphoid cell; iNKT, innate natural killer T cell; MetEnk, methionine-enkephalin peptides; NK, natural killer cell