Investigate the innate and adaptive immune systems in mammals, including the response of animal adaptive immunity to infection (third line of defence: humoral and cell-mediated immunity, including the roles of lymphocytes, antibodies and antigens)

What this dot point is asking

NESA wants you to describe the third line of defence in mammals: the adaptive (specific) immune response. You must cover both humoral (B-cell, antibody-mediated) and cell-mediated (T-cell) immunity, name the lymphocyte types, and explain memory cells and the secondary response. This is among the highest-value Module 7 dot points and appears in nearly every extended-response question.

The answer

Adaptive immunity is specific (each lymphocyte recognises one antigen) and has memory (faster, larger response on re-exposure). It develops over 5 to 14 days during a first infection.

Antigens and antigen presentation

An antigen is any molecule (usually a protein or polysaccharide) that triggers an adaptive immune response. Antigen-presenting cells (APCs) including macrophages and dendritic cells engulf pathogens, digest them, and display fragments on MHC class II molecules. Infected cells display intracellular antigen fragments on MHC class I.

Lymphocyte types

All lymphocytes mature into one of three classes.

B lymphocytes (B cells). Mature in the bone marrow. Each B cell has a unique surface antibody (B-cell receptor) that recognises one antigen.

T lymphocytes (T cells). Mature in the thymus. Each T cell has a unique T-cell receptor (TCR) that recognises one antigen displayed on MHC. Two main subtypes:

• Helper T cells (CD4) recognise antigen on MHC class II. They coordinate the response by secreting cytokines.
• Cytotoxic T cells (CD8) recognise antigen on MHC class I. They kill infected cells.

Memory cells. A subset of activated B and T cells become long-lived memory cells.

Humoral immunity (B cells and antibodies)

Targets pathogens in body fluids.

1. A B cell binds its specific antigen.
2. With help from a matching helper T cell (which has recognised the same antigen on MHC class II), the B cell becomes activated.
3. The activated B cell undergoes clonal expansion, producing many identical daughter cells.
4. Most daughter cells become plasma cells, secreting around 2000 antibodies per second specific to that antigen. A fraction become memory B cells.

Antibodies (immunoglobulins). Y-shaped proteins with two antigen-binding sites. Functions:

• Neutralisation. Bind viruses or toxins, blocking their attachment to host cells.
• Agglutination. Clump pathogens together, easing phagocytosis.
• Opsonisation. Mark pathogens for phagocytes that have antibody receptors.
• Complement activation. Trigger the complement cascade, leading to membrane lysis.

The five antibody classes are IgM (first produced), IgG (most abundant, longest-lasting), IgA (mucosal), IgE (allergies and parasites) and IgD (B-cell receptor).

Cell-mediated immunity (T cells)

Targets infected, cancerous or abnormal host cells.

1. An infected cell displays a viral or abnormal peptide on MHC class I.
2. A cytotoxic T cell with a matching TCR binds the MHC-peptide complex.
3. The cytotoxic T cell releases perforin (forms pores in the target's membrane) and granzymes (proteases that trigger apoptosis), destroying the infected cell.

Helper T cells coordinate the wider response. They release cytokines such as interleukin-2 that activate cytotoxic T cells, stimulate B-cell proliferation, and enhance macrophage activity.

Primary and secondary responses

Primary response. First exposure to a pathogen. Takes 5 to 14 days to produce significant antibody. Symptoms may develop while immunity is building.

Secondary response. Re-exposure to the same pathogen. Memory cells recognise the antigen within hours. Antibody production is faster, higher and longer-lasting. Disease is often prevented or reduced to subclinical levels. This is the basis of natural immunity and vaccination.

Worked example

A child receives a measles vaccine at 12 months. Five years later, the child is exposed to measles in a classroom outbreak.

At vaccination. Attenuated measles antigens are processed by APCs. Helper T cells and B cells specific for measles are activated. After 1 to 2 weeks, IgG antibodies are produced and memory B and T cells form.

On re-exposure. Within 1 to 2 days, memory B cells differentiate into plasma cells, producing large amounts of IgG. Memory cytotoxic T cells destroy infected cells. The virus is cleared before significant disease develops. The child remains asymptomatic.

Common traps

Confusing B and T cells. B cells produce antibodies. T cells kill infected cells (cytotoxic) or coordinate the response (helper).

Forgetting MHC. T cells cannot recognise free antigen. They only recognise antigen presented on MHC molecules.

Saying antibodies kill pathogens directly. Antibodies usually do not kill. They neutralise, agglutinate, opsonise, or trigger complement, which then kills.

Skipping helper T cells. Without helper T-cell activation, B cells generally cannot make a strong response. Markers expect helper T cells to be named.

Confusing memory cells with active plasma cells. Plasma cells secrete antibody during the response and then die within weeks. Memory cells do not secrete antibody but persist for years, ready to respond on re-exposure.

In one sentence

The adaptive immune response uses B lymphocytes (which differentiate into plasma cells secreting specific antibodies) for humoral immunity, and T lymphocytes (helper T cells coordinating the response, cytotoxic T cells killing infected cells) for cell-mediated immunity, and produces long-lived memory cells that mount a faster and larger secondary response on re-exposure.