Phagocytosis & Phagocytic Cells
Phagocytosis
Primary innate mechanism for removing pathogens and cellular debris
Sequence: recognition → engulfment → intracellular killing
Links innate and adaptive immunity (antigen presentation by macrophages)
Phagocytic Cell Types
Neutrophils
First leukocytes to arrive (within hours)
Rapid phagocytosis and release of cytotoxic granules
Short-lived; form pus
Monocytes
Circulate in blood; migrate after ≈ days
Differentiate into macrophages at infection sites
Macrophages
Tissue-resident or derived from monocytes
Long-lived; high phagocytic capacity
Secrete cytokines, present antigen, orchestrate inflammation
Pathogen Recognition
Two strategies
Opsonization: pathogen coated by opsonins (antibody, complement, C-reactive protein) → easier uptake
Direct PAMP detection: phagocyte Pattern Recognition Receptors (PRRs) bind Pathogen-Associated Molecular Patterns (PAMPs)
Key PAMP examples
Peptidoglycan, LPS, flagellin, lipopeptides, viral DNA/RNA
Toll-Like Receptors (TLRs) (subset of PRRs)
Cell-surface TLRs 1, 2, 4, 5, 6 detect bacterial envelope components
Endosomal TLRs 3, 7, 8, 9 detect viral/bacterial nucleic acids
PRR–PAMP binding activates phagocyte → ↑phagocytosis, cytokine/IFN production, proliferation, killing efficiency
Chemotaxis & Diapedesis (Extravasation)
Chemotaxis: movement along chemical gradient (cytokines, complement )
Rolling adhesion: cytokines induce endothelial adhesion molecules; leukocytes slow & roll
Transendothelial migration/Diapedesis: leukocytes squeeze between capillary cells into tissue
Arrival hierarchy: neutrophils → monocytes → macrophages (resident macrophages already present)
Process occurs only in capillaries (thin walls, low flow)
Key Takeaways
Phagocytosis requires pathogen recognition; PRRs provide opsonin-independent detection
PAMP–PRR interaction is both recognition and activation signal
Efficient immune response depends on rapid chemotaxis/diapedesis bringing vast numbers of phagocytes to the infection site