Macrophages and Inflammation

Inflammation is a normal physiological response to an infection or injury, such as aggression by microbes, trauma, or heat and radiation. Inflammation works to maintain homeostasis and is a highly regulated process with both pro- and anti-inflammatory components to ensure the prompt resolution of noxious conditions. In the initial stages of inflammation, macrophages destroy the abnormal stimuli, and remove the apoptotic bodies of the dead neutrophils as well as any remaining hazard factor. The macrophages then present the antigen to T lymphocytes to initiate the mechanisms of acquired immunity, which leads to the production of antibodies, cytokines and memory cells. The macrophage activity then switches from proinflammatory to antiinflammatory to remove any elements of aggression, thereby achieving homeostasis. Macrophages play a key role in the innate immune response and form a bridge between the innate and acquired immune response. In certain circumstances, however, when chronic inflammation is produced, macrophages may have a harmful effect and cause lesions. Therefore, inflammation is the classic “double-edged sword”, in which macrophages cut both ways. Activated macrophages have two different phenotypes related to different stimuli: M1 (classically activated) and M2 (alternatively activated). M1 macrophages are proinflammatory and play a key role in the host defense mechanism, while M2 are associated with the responses to anti-inflammatory reactions and tissue remodeling. The transformation of different phenotypes of macrophages regulates the initiation, development, and cessation of inflammatory diseases. An imbalance of macrophage M1∼ M2 polarization is often associated with a range of diseases or inflammatory conditions, such as rheumatoid arthritis and systemic lupus erythematous. (J Rheum Dis 2018;25:11-18)