Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or immature dendritic cells. Non-professional phagocytes such as epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes.
Normal cells contain receptors that prevent them from being recognized by phagocytes. For example, red blood cells display CD47 receptors that block phagocytosis. Another marker, CD31, also known as platelet endothelial cell adhesion molecule-1, is expressed by normal cells, which prevents phagocyte attachment. During apoptosis, CD31 is not expressed, leading to phagocyte recognition and phagocytosis.
Apoptotic cells release 'find-me' signals such as lysophosphatidylcholine, sphingosine-1-phosphate, fractalkine, thrombospondin-1, ATP, and UTP to help phagocyte recognition. Once the phagocytes reach the location, the apoptotic cells display 'eat-me' signals, such as apoptotic cell-associated molecular patterns (ACAMP) and phosphatidylserine. When phagocytes attach to apoptotic cells, they release anti-inflammatory cytokines such as IL-10 and TGF-ꞵ, creating a non-inflammatory microenvironment. This prevents damage to neighboring cells. Once the apoptotic cells are internalized, they are broken down into nucleotides, amino acids, and sterols which are further recycled.
