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Abstract
It has long been known that adipose tissue in obesity is in a heightened state ofinflammation. Recently, our understanding of this has been transformed by the knowledgethat immune cells such as macrophages and T cells can infiltrate adipose tissue and areresponsible for the majority of inflammatory cytokine production. These seminal findingshave opened up a new area in biology that is garnering the interest of scientists involved inresearch relating to cell motility, inflammation, obesity, physiology, diabetes andcardiovascular disease. Some important general questions relevant to this field are: how are macrophages recruited to adipose tissue in obesity? What are the physiologicalconsequences of macrophage—adipocyte interactions? Do these inflammatory macrophages contribute to pathophysiological conditions associated with obesity, such asinsulin resistance, dyslipidemia, diabetes and cardiovascular disease? This review focuseson the first of these important questions.
