Hypothetical model of macrophage–T-cell interactions in adipose tissue during obesity. Diet-induced obesity upregulates MHC-II
expression on ATMs, which process the antigens (Ag) and present them to CD4 cells via MHC-TCR interaction. Obesity-induced
upregulation of costimulatory molecules (CD80/86) on ATMs and interaction with the T-cell CD28 molecule sustains effector
T-cell proliferation. The obesity-induced antigen-specific immune response upregulates T-cell–derived Thelper1 (Th1) cytokines
IL-2 and interferon-γ (IFN-γ). IL-2 in concert with other adipokines, such as leptin, may promote T-cell proliferation, whereas
IFN-γ can induce macrophage activation and act on adipocytes to induce effector immune response in adipose tissue.