<P> Macrophages are the predominant cells involved in creating the progressive plaque lesions of atherosclerosis . </P> <P> Focal recruitment of macrophages occurs after the onset of acute myocardial infarction . These macrophages function to remove debris, apoptotic cells and to prepare for tissue regeneration . </P> <P> Macrophages also play a role in human immunodeficiency virus (HIV) infection . Like T cells, macrophages can be infected with HIV, and even become a reservoir of ongoing virus replication throughout the body . HIV can enter the macrophage through binding of gp120 to CD4 and second membrane receptor, CCR5 (a chemokine receptor). Both circulating monocytes and macrophages serve as a reservoir for the virus . Macrophages are better able to resist infection by HIV - 1 than CD4+ T cells, although susceptibility to HIV infection differs among macrophage subtypes . </P> <P> Macrophages can contribute to tumor growth and progression by promoting tumor cell proliferation and invasion, fostering tumor angiogenesis and suppressing antitumor immune cells . Attracted to oxygen - starved (hypoxic) and necrotic tumor cells they promote chronic inflammation . Inflammatory compounds such as tumor necrosis factor (TNF) - alpha released by the macrophages activate the gene switch nuclear factor - kappa B. NF - κB then enters the nucleus of a tumor cell and turns on production of proteins that stop apoptosis and promote cell proliferation and inflammation . Moreover, macrophages serve as a source for many pro-angiogenic factors including vascular endothelial factor (VEGF), tumor necrosis factor - alpha (TNF - alpha), Macrophage colony - stimulating factor (M - CSF / CSF1) and IL - 1 and IL - 6 contributing further to the tumor growth . Macrophages have been shown to infiltrate a number of tumors . Their number correlates with poor prognosis in certain cancers including cancers of breast, cervix, bladder, brain and prostate . Tumor - associated macrophages (TAMs) are thought to acquire an M2 phenotype, contributing to tumor growth and progression . Some tumors can also produce factors, including M - CSF / CSF1, MCP - 1 / CCL2 and Angiotensin II, that trigger the amplification and mobilization of macrophages in tumors . Research in various study models suggests that macrophages can sometimes acquire anti-tumor functions . For example, macrophages may have cytotoxic activity to kill tumor cells directly; also the co-operation of T - cells and macrophages is important to suppress tumors . This co-operation involves not only the direct contact of T - cell and macrophage, with antigen presentation, but also includes the secretion of adequate combinations of cytokines, which enhance T - cell antitumor activity . Recent study findings suggest that by forcing IFN - α expression in tumor - infiltrating macrophages, it is possible to blunt their innate protumoral activity and reprogram the tumor microenvironment toward more effective dendritic cell activation and immune effector cell cytotoxicity . Additionally, subcapsular sinus macrophages in tumor - draining lymph nodes can suppress cancer progression by containing the spread of tumor - derived materials . </P>

Active phagocytes that become macrophages in the the tissue