Aging is associated with a number of chronic diseases – cardiovascular disease, diabetes, Alzheimer’s disease and other dementias, and cancer. They are all part of the process of immunosenescence. The chronic inflammation that is a feature of the declining efficiency of geriatric immune systems has a deleterious effect on normal metabolic and hormonal signaling, is increased by the accumulation of cell debris as we age (for instance in the eye), and is typified by chronically elevated levels of circulating pro-inflammatory cytokines.These processes are well reviewed in a recent paper in the journal Aging Mechanisms and Disease, titled “Macrophages in age-related chronic inflammatory diseases”, by Yumiko Oishi and Ichiro Manabe. These chronic inflammatory processes, say the authors, tend not to be dramatic but are long-term, low-grade smouldering responses to things like tissue repair and insult by pathogens. And changes in the behavior of macrophages in particular, as we age, are central to driving inflammation. Macrophages, they say, not only promote inflammation and tissue dysfunction but also are essential for resolution and healing of inflammation, as well as maintenance of tissue homeostasis. But, as we age, while macrophages turn on the inflammation that underlies healing processes and resistance to infection, they become less good at turning inflammation off when it has done its job. Thus macrophages appear to contribute crucially to the paradoxical activation of basal chronic inflammatory states in the elderly and to the progression of age-associated diseases.