This section will help you better understand the mechanisms of phagocytosis, a key step in innate immunity. Phagocytosis involves specialized cells called phagocytes, which neutralize pathogens such as bacteria. Several immune cells are capable of phagocytosis, particularly macrophages, dendritic cells, and granulocytes. Pathogens carry molecular patterns on their surface that are recognized by phagocytes. These membrane markers, common to many pathogens, are called PAMPs (polymorphonuclear antigen-binding proteins). Examples include bacterial cell wall lipopolysaccharides (LPS) and beta-glucans. These molecules are recognized by phagocytes via PRR (polymorphonuclear receptor) membrane receptors. Examples include scavenger receptors and TLRs (transient receptors). Some phagocytes also possess receptors for the FC (frontal cortex) portion of antibodies. When antibodies bind to the membrane antigens of pathogens, the phagocyte then binds to the Fc region of the antibodies to promote phagocytosis in a process called opsonization.
In the absence of antibodies, pathogens bind to PRR receptors, which triggers an invagination mechanism of the foreign element into the phagocyte, which surrounds it using its pseudopodia, leading to endocytosis.
Once inside the phagocyte, the foreign element enters the phagosome. The macrophage possesses vesicles, or lysosomes, filled with lytic enzymes: lysozyme. These enzymes are capable of degrading the pathogen trapped within the phagosome. The lysosomes fuse with the phagosome membrane to release their lytic enzymes. The complex then forms what is called a phagolysosome. The release of lysozyme leads to the digestion of the pathogen into multiple small fragments, or antigenic peptides. The waste products are then expelled through exocytosis.
Within the macrophage, other vesicles contain MHC, or major histocompatibility complex, molecules. These are MHC class II molecules. The antigenic peptides bind to the MHC molecules to be presented to other cells of the immune system. The macrophage thus becomes an antigen-presenting cell, enabling the triggering of the adaptive immune response.