Makrofaagid

Makrofaagid, or macrophages, are a diverse group of immune cells that form part of the innate immune system. In the body they reside in tissues and originate from monocytes that develop in the bone marrow. Once they migrate into tissues, monocytes differentiate into macrophages, adapting to local environments. Macrophages perform phagocytosis, engulfing bacteria, dead cells, and debris, and they clear apoptotic cells through efferocytosis. They also act as professional antigen-presenting cells by presenting processed antigens on MHC class II molecules to CD4+ T cells, thereby linking innate and adaptive immunity. In addition, they secrete cytokines and chemokines that regulate inflammation and recruit other immune cells.

Macrophages display functional plasticity. In response to signals such as IFN-γ and microbial products, they can become classically activated (M1), producing pro-inflammatory cytokines and antimicrobial effectors. In contrast, signals like IL-4 and IL-13 promote alternative activation (M2), which support tissue repair, anti-inflammatory responses, and remodeling. In vivo, many macrophages exhibit mixed phenotypes and tissue-specific programs.

Many tissues host resident macrophages with specialized roles: alveolar macrophages in the lung clear inhaled particles; Kupffer cells in the liver monitor blood-borne material; microglia in the brain survey the neural environment; osteoclasts, derived from macrophages, are involved in bone resorption. Macrophages also contribute to iron metabolism and clearance of senescent red blood cells.

Macrophages are central to several diseases. In atherosclerosis they ingest lipids and form foam cells; in cancer, tumor-associated macrophages can promote or hinder tumor growth depending on their state; defective efferocytosis and chronic activation contribute to inflammatory and fibrotic diseases.

Understanding macrophage biology informs therapies targeting inflammation, infection, and tissue repair, including strategies to reprogram macrophage function or deplete pathogenic populations.