Fagosytointia

Fagosytointi, or phagocytosis, is a cellular process in which certain cells, notably professional phagocytes such as macrophages, neutrophils, and dendritic cells, ingest and degrade particulate material, including bacteria, viruses, dead or dying cells, and debris. It is a key mechanism of innate immunity and also contributes to the initiation of adaptive immune responses.

The process begins with recognition and attachment. Phagocytes detect particles through pattern recognition receptors that bind common microbial components, and through opsonins such as antibodies and complement that tag targets for ingestion. Following binding, the cell membrane engulfs the particle, forming a phagosome. The phagosome then matures by fusing with lysosomes to become a phagolysosome, where acidic conditions, hydrolytic enzymes, and antimicrobial peptides break down the contents. An oxidative burst, generated by NADPH oxidase, produces reactive oxygen species that help kill ingested microbes. In many cells, degraded material is loaded onto MHC class II molecules and presented to T cells, linking innate and adaptive immunity.

Cells involved in fagosytointi include professional phagocytes, though non-professional phagocytes can also participate under certain conditions. Regulation of phagocytosis is essential for host defense, tissue remodeling, and maintenance of homeostasis through clearance of apoptotic cells.

Clinical relevance includes increased infection risk with defects in phagocyte function or the oxidative burst, such as chronic granulomatous disease. Impaired opsonization or receptor signaling can also compromise microbial clearance and clearance of cellular debris, contributing to inflammatory or autoimmune processes. Conversely, excessive phagocytic activity may contribute to tissue damage in certain inflammatory conditions.