the innate immune response, including physical, chemical and microbiological barriers and the inflammatory response; and the adaptive immune response, including the roles of B cells, T cells (helper and cytotoxic), antibodies, antigens, and immunological memory

What this dot point is asking

VCAA wants the innate immune response (barriers, inflammation, phagocytes) and the adaptive immune response (B cells, T cells, antibodies, memory), including the humoral and cell-mediated branches, and the key difference: specificity and memory.

The answer

The immune system has two branches that work together: the innate response (fast, non-specific, no memory) and the adaptive response (slower, specific, with memory).

The innate immune response

The innate system is the first line of defence. It is present from birth, acts within minutes to hours, and treats every pathogen the same way.

Physical barriers.

• Skin. Tough, dry outer layer (keratinised dead cells) that few pathogens can penetrate.
• Mucous membranes. Line the respiratory, digestive, urogenital and reproductive tracts. Mucus traps pathogens.
• Cilia. In the respiratory tract, cilia sweep trapped pathogens up to be coughed, sneezed or swallowed.
• Tears, urine flow and peristalsis. Physically wash pathogens away.

Chemical barriers.

• Stomach acid (pH about 2) kills most bacteria in food.
• Lysozyme in tears, saliva and mucus digests bacterial cell walls.
• Antimicrobial peptides (defensins) on the skin and in mucus.
• Sebum on the skin lowers pH and inhibits bacterial growth.

Microbiological barriers.

• The normal microbiota (commensal bacteria on the skin, in the gut and elsewhere) compete with pathogens for space and nutrients and produce antimicrobial substances.

Cells of innate immunity.

• Neutrophils. Most common white blood cell; first to arrive at infection; phagocytose bacteria.
• Macrophages. Larger phagocytes that engulf pathogens and present antigens to T cells, linking innate to adaptive immunity.
• Dendritic cells. Specialised antigen-presenting cells; capture pathogens and carry them to lymph nodes.
• Natural killer (NK) cells. Destroy virus-infected and cancerous cells by triggering apoptosis.
• Mast cells. Release histamine, triggering inflammation.

The inflammatory response. When tissue is damaged or infected, mast cells release histamine and cytokines, causing:

1. Vasodilation. Blood vessels widen, increasing blood flow (redness, heat).
2. Increased permeability. Plasma leaks into tissue (swelling).
3. Chemotaxis. Phagocytes are attracted to the site.
4. Phagocytosis. Pathogens are engulfed and digested.
5. Pain. Pressure on nerves and chemicals like prostaglandins.

Systemic responses include fever (cytokines reset the hypothalamic thermostat) and leukocytosis (increased white blood cell count).

The adaptive immune response

The adaptive system is specific (targets one pathogen), takes days to mount on first exposure, and produces memory so the second exposure is much faster and stronger.

Antigen presentation. Dendritic cells, macrophages and B cells engulf pathogens, break them down and display fragments (antigens) on MHC class II molecules on their surface. Infected body cells display fragments of internal pathogens on MHC class I molecules.

Clonal selection. Each B cell and T cell carries one specific receptor. When the receptor matches a presented antigen, the cell is selected, activated and proliferates (clonal expansion).

Helper T cells (CD4+). Bind antigen on MHC class II. Once activated, they secrete cytokines that coordinate the rest of the adaptive response: activating cytotoxic T cells, stimulating B cell proliferation, and amplifying macrophage activity.

Cytotoxic T cells (CD8+). Bind antigen on MHC class I (on infected body cells). They release perforin (which makes pores in the target cell membrane) and granzymes (which trigger apoptosis), killing the infected cell. This is cell-mediated immunity.

B cells. Bind free antigen using their B cell receptor (a membrane-bound antibody). With help from helper T cells, they differentiate into:

• Plasma cells. Antibody factories. Secrete huge numbers of soluble antibodies into the blood and lymph.
• Memory B cells. Long-lived cells that respond rapidly to future infections.

This is humoral immunity.

Antibodies (immunoglobulins). Y-shaped proteins with two antigen-binding sites specific to one antigen. They work by:

• Neutralisation. Block pathogens from binding to host cells.
• Agglutination. Clump pathogens together so they can be phagocytosed.
• Opsonisation. Coat pathogens, making them easier for phagocytes to engulf.
• Activating the complement cascade. Triggers lysis of pathogens.

The main classes are IgG (most abundant in blood), IgM (first to appear, large pentamer), IgA (in mucus and milk), IgE (allergies and parasites) and IgD (B cell receptor).

Memory and the secondary response. After the infection is cleared, most effector cells die. Memory B and T cells persist for years. If the same pathogen is encountered again, the secondary response is:

• Faster (days instead of weeks).
• Larger (more antibodies and effector cells).
• More targeted (higher-affinity antibodies due to affinity maturation).

This is the basis of immunity after natural infection or vaccination.

Comparing innate and adaptive

The two branches communicate constantly. Antigen-presenting cells of the innate system trigger the adaptive response, and cytokines from adaptive cells amplify innate functions.

Worked example

A child catches measles for the first time. Day 1: virus enters via the respiratory tract. Innate responses (mucus, ciliary clearance, alveolar macrophages, NK cells, inflammation) slow but cannot clear the infection. Day 4: dendritic cells carry viral antigens to a lymph node. Helper T cells with matching receptors are activated and produce cytokines. Cytotoxic T cells kill infected cells; B cells differentiate into plasma cells and start making antibodies. Day 10: antibody levels peak; the rash appears as the immune system attacks infected skin cells. Day 14: virus is cleared. Memory B and T cells persist for life. If the child encounters measles again, the secondary response clears the virus before symptoms develop. The child is immune.

Common traps

Saying B cells make antibodies on first contact within hours. B cells need helper T cell signals and several days to differentiate into plasma cells. The first response is slow.

Confusing cell-mediated and humoral immunity. Cell-mediated = cytotoxic T cells kill infected body cells. Humoral = B cells and antibodies act on extracellular pathogens.

Saying the innate response is "weak". It is non-specific but very effective at clearing most invaders before the adaptive response is needed.

Calling all white blood cells "lymphocytes". Only B cells, T cells and NK cells are lymphocytes. Neutrophils, macrophages and dendritic cells are not.

Forgetting MHC. T cells only recognise antigens that are presented on MHC molecules, not free in solution.

In one sentence

The innate immune response provides rapid, non-specific defence through physical and chemical barriers (skin, mucus, stomach acid, lysozyme), normal microbiota, phagocytes (neutrophils, macrophages, dendritic cells), NK cells and the inflammatory response, while the adaptive response provides slower but specific defence with memory: helper T cells coordinate the response, cytotoxic T cells kill infected body cells (cell-mediated immunity), B cells differentiate into plasma cells that secrete antibodies against extracellular pathogens (humoral immunity), and memory B and T cells produce a faster, larger response on re-exposure.