Describe the lines of defence against pathogens, including non-specific defences and the specific immune response with B and T lymphocytes

What this dot point is asking

WACE wants you to organise the immune system into a layered defence and to explain how the specific response recognises and remembers particular pathogens. Pathogens are disease-causing agents and you should know the main types: bacteria, viruses, fungi, protozoa and other parasites, and prions. Each carries antigens, molecules on its surface that the immune system can recognise as non-self.

The first line of defence (non-specific, external)

The first line stops pathogens entering and is non-specific, meaning it acts against anything regardless of type. It includes physical barriers such as the skin and the cilia and mucus lining the airways, and chemical barriers such as stomach acid, lysozyme in tears and saliva, and the slightly acidic skin surface. Useful microorganisms (the normal flora) also compete with pathogens. If these barriers are intact, most pathogens never get inside.

The second line of defence (non-specific, internal)

If a pathogen breaches the barriers, the second line responds, still without targeting a specific pathogen. Its key features are:

• Phagocytosis: white blood cells called phagocytes (for example macrophages and neutrophils) engulf and digest pathogens.
• Inflammation: damaged cells release histamine, blood vessels dilate and become more permeable, and the area becomes red, warm, swollen and painful as more white cells and plasma arrive.
• Fever: the hypothalamus raises the temperature set point, which slows pathogen reproduction and speeds immune activity.
• Other defences: complement proteins and interferons (which interfere with viral replication) support the response.

The third line of defence (specific immune response)

The third line is specific: it targets a particular pathogen by recognising its antigens, and it produces memory. It has two arms, both involving lymphocytes (a type of white blood cell) made in the bone marrow.

Humoral (antibody-mediated) immunity is driven by B lymphocytes. When a B cell with the matching receptor meets its antigen (often presented by a helper T cell), it is activated and divides into many plasma cells that secrete antibodies. Antibodies bind to the antigen and neutralise the pathogen, clump pathogens together (agglutination), or mark them for phagocytosis.

Cell-mediated immunity is driven by T lymphocytes, which mature in the thymus. Helper T cells release chemicals (cytokines) that activate B cells and other T cells. Cytotoxic (killer) T cells destroy the body's own cells that are infected by viruses or that have become cancerous.

Immunological memory and immunity

The first (primary) response is slow because the matching lymphocytes are rare and must be selected and multiplied. Memory B and T cells made during this response survive long term. On a second exposure to the same antigen, these memory cells trigger a secondary response that is faster and produces far more antibody, often stopping the disease before symptoms appear. This is the basis of long-lasting immunity.

You also need active versus passive immunity:

• Active immunity is when the person's own immune system makes antibodies and memory cells, either by catching the disease (natural) or by vaccination (artificial). It is slow to develop but long-lasting.
• Passive immunity is when ready-made antibodies are received from another source, such as across the placenta or in breast milk (natural) or by injection of antibodies (artificial). It is immediate but temporary, because no memory cells form.

How this maps to the exam

Expect questions that ask you to place a defence in the correct line, distinguish non-specific from specific defences, explain why the secondary response is faster, or compare active and passive immunity in the context of vaccination. Use precise terms: phagocyte, lymphocyte, antigen, antibody, plasma cell and memory cell.