The concept that atherosclerosis is a chronic inflammatory disease is now widely accepted1). Interestingly, leukocyte infiltration into atherosclerotic lesions had already been described by the middle of the 19th century, and Rudolf Virchow suggested that inflammation and/or infiltration by leukocytes may directly contribute to the pathogenesis of atherosclerosis2). Moreover, it was more than a century ago that Williamson et al. reported that the administration of sodium salicylate reduces the urinary sugar level, thus suggesting that inflammation is also involved in diabetes3). After these pioneering works, however, inflammation and the role of immune cells in cardiovascular and metabolic disease were largely neglected for decades. In contrast, today, chronic inflammation is recognized to be a key player in the pathogenesis of cardiometabolic disease, including both atherosclerosis and type 2 diabetes (T2D). Indeed, the emerging field of immunometabolism, which explores the interplay between immunological and metabolic processes, focuses on the pathological mechanisms underlying various noncommunicable diseases (NCDs), including Alzheimer’s disease, renal disease and cancer, in addition to cardiometabolic disease4-7). Clinically, the circulating levels of proinflammatory cytokines, such as tumor necrotic factor-α (TNF-α), interleukin-6 (IL-6), IL-1β and IL-18, are elevated in patients with chronic heart failure, positively correlating with the disease severity8). Similarly, a high level of C-reactive protein (CRP) is an independent risk factor for cardiovascular disease9), while elevated CRP, IL-6, fibrinogen and plasminogen activator inhibitor-1 (PAI-1) levels, as well as an increased white blood cell count, associate with T2D10, 11). Notably, the levels of these inflammatory markers can be reversed by improvements in lifestyle12). Taken together, these findings strongly suggest that chronic inflammation is crucially involved in the development