The Innate Immune System

• Q1 — C: The defining distinction is specificity of recognition: innate immunity uses PRRs to detect PAMPs — broad molecular patterns shared by many pathogens (e.g. bacterial LPS, viral RNA). Adaptive immunity uses antigen-specific receptors (BCR, TCR) that recognise a single specific antigen. Both systems use white blood cells (A is wrong). Adaptive immunity evolved in vertebrates (B is reversed). Both operate in blood and tissues (D is wrong).
• Q2 — B: A phagolysosome forms when a lysosome (containing digestive enzymes including proteases, lipases, and lysozyme) fuses with the phagosome (the vesicle containing the engulfed pathogen). Pseudopod extension (A) creates the phagosome — a separate prior step. Antigen presentation (C) occurs after digestion. PRR binding (D) is the adherence step — before ingestion.
• Q3 — D: NK cells detect the absence of MHC class I — the "missing self" signal. Many viruses reduce MHC I expression to hide from cytotoxic T cells; this makes them visible to NK cells. NK cells do not use PRRs to detect viral PAMPs on cell surfaces (A) — that's macrophage/neutrophil function. Antibody-coating (B) describes antibody-dependent cellular cytotoxicity — a different mechanism involving specific antibodies. Interferons activate NK cells (C) but do not mark infected cells for destruction in the way described.
• Q4 — A: Dendritic cells bridge both systems: they engulf pathogens (innate phagocytosis), process antigens, then migrate to lymph nodes where they present fragments on MHC II to naive T cells — activating the adaptive response. They do not produce antibodies (B). They do not directly activate B and T cells without antigen presentation (C). They are found in tissues as part of the innate system; the adaptive system operates in lymphoid organs and blood (D is misleading).
• Q5 — C: Perforin is the pore-forming protein used by NK cells and cytotoxic T cells to puncture target cell membranes — initiating cell death. Without perforin, neither cell type can kill virus-infected cells or tumours effectively. Perforin is not involved in histamine release (A — mast cells), pseudopod formation in phagocytosis (B — actin cytoskeleton), or complement activation (D — complement has its own activation pathway).

SA1: Neutrophils target pathogens directly — primarily bacteria and fungi that are present in the extracellular space or have entered the tissue. They identify their targets using pattern recognition receptors (PRRs) on their surface that bind pathogen-associated molecular patterns (PAMPs) — for example, LPS on gram-negative bacterial cell walls. Once adherence is achieved, neutrophils destroy the pathogen through phagocytosis: they engulf it into a phagosome, which fuses with a lysosome to form a phagolysosome containing digestive enzymes and reactive oxygen species that destroy the pathogen. Natural killer cells target infected host cells — cells that have already been colonised by a virus and are being used for viral replication. They identify their targets not by the presence of a foreign molecule, but by the absence of a normal one: healthy cells display MHC class I on their surface; virus-infected and cancerous cells often reduce or lose MHC I expression. NK cells detect this "missing self" signal and destroy the target cell by releasing perforin (which punches holes in the target cell membrane) and granzymes (proteolytic enzymes that enter through the perforin pores and trigger apoptosis). The key difference is target: neutrophils destroy the pathogen itself, while NK cells destroy the host cell that the pathogen is hiding inside.

SA2: When a phagocyte detects a pathogen, pattern recognition receptors (PRRs) on the phagocyte surface bind to PAMPs on the pathogen — this is the adherence step. The phagocyte then extends membrane projections called pseudopods around the pathogen, engulfing it and enclosing it in a membrane-bound vesicle called a phagosome. The phagosome then fuses with a lysosome — an organelle containing a concentrated mixture of digestive enzymes (including proteases, lipases, and lysozyme) and reactive oxygen species. The fused structure is called a phagolysosome. Inside, the enzymes break down the pathogen's structural components — proteins, lipids, nucleic acids — destroying it. After digestion, fragments of the pathogen's proteins (antigens) are loaded onto MHC class II molecules and transported to the phagocyte's surface, where they are displayed for recognition by T helper cells — initiating the adaptive immune response.

SA3: When bacteria breach the skin through a wound, the following innate immune sequence occurs. Mast cells in the surrounding connective tissue detect bacterial PAMPs and immediately release histamine, causing vasodilation and increased capillary permeability — producing the redness, warmth, and swelling of early inflammation, and delivering immune molecules to the site in leaked plasma. Complement proteins circulating in the blood are activated by contact with bacterial surface molecules — they coat the bacteria (opsonisation, making them easier to phagocytose), release chemokines that attract neutrophils, and can directly attack bacterial membranes via the membrane attack complex. Neutrophils, attracted by the chemokine gradient, exit the bloodstream through capillary walls (diapedesis) and phagocytose the bacteria — engulfing them into phagosomes, fusing lysosomes to form phagolysosomes, and destroying the bacteria with digestive enzymes and reactive oxygen species. Macrophages already resident in the tissue also phagocytose bacteria and release cytokines (IL-1, IL-6, TNF-alpha) that signal systemically — triggering fever via the hypothalamus, recruiting additional immune cells, and activating dendritic cells. Dendritic cells engulf bacterial antigens, process them, and begin migrating to lymph nodes — where they will initiate the adaptive immune response by presenting antigens to naive T cells.