11. Immunity
- Syllabus
- 9700–2028–2029
- Section
- 11
- Level
- AS
Exam analysis
Most tested topics
11.1 The Immune System
- Syllabus
- 9700–2028–2029
- Topic
- 11.1
- Level
- AS
Phagocytes engulf, digest and expose pathogen evidence
Macrophages and neutrophils are phagocytes: they provide an immediate, non-specific defence by recognising, engulfing and digesting pathogens.
- Chemicals released by pathogens or damaged tissue attract the phagocyte by chemotaxis.
- Surface receptors attach to molecules on the pathogen.
- The cell membrane surrounds the pathogen and encloses it in a phagosome.
- Lysosomes fuse with the phagosome; hydrolytic enzymes digest the pathogen.
- Useful products may be absorbed or released, while waste is removed.
| Phagocyte | Additional role |
|---|---|
| Neutrophil | Rapidly enters infected tissue, phagocytoses pathogens and is often short-lived |
| Macrophage | Longer-lived; after digestion, displays pathogen antigen fragments with cell-surface molecules and acts as an antigen-presenting cell |
Antigen presentation follows digestion of the pathogen: the macrophage displays selected antigen fragments, not an intact pathogen it deliberately failed to destroy. Phagocytes do not secrete pathogen-specific antibodies.
Antigens let the immune system distinguish self from non-self
An antigen is a molecule that can be recognised by the immune system and can stimulate a specific immune response when recognised as non-self. Antigens are often proteins or glycoproteins on cell or pathogen surfaces.
| Antigen class | Origin and normal immune consequence |
|---|---|
| Self antigen | Produced by the body's own cells; immune tolerance normally prevents a response against it |
| Non-self antigen | Foreign to the body, for example on a pathogen or transplanted cell; recognition can activate specific lymphocytes |
Different antigens have different molecular shapes. Only an antibody or lymphocyte receptor with a complementary binding site recognises a particular antigen, which gives the later immune response its specificity.
An antigen is not necessarily the whole pathogen and is not defined only as a marker for ordinary cell-to-cell recognition. 'Self' describes origin and immune tolerance; it does not mean the molecule lacks a shape or identity.
The primary immune response selects and expands specific B and T lymphocytes
A primary immune response is the specific response to a newly encountered non-self antigen. Antigen presentation selects lymphocytes with complementary receptors, which then divide and differentiate into cells that act against the pathogen or infected body cells.
- A macrophage presents pathogen antigen fragments; antigens may also be displayed on a pathogen or an infected body cell.
- The B- and T-lymphocytes with receptors complementary to the antigen are selected. This is clonal selection.
- The selected lymphocytes divide by mitosis, producing many clones with the same antigen specificity. This is clonal expansion.
- B-cell clones form plasma cells, which secrete antibodies complementary to the antigen. T-cell clones form T-helper cells that stimulate B-cell division and T-killer cells that attach to infected cells and kill them.
- The antibody response and T-killer action help remove the pathogen or infected cells. The first response is slow because selection, expansion and differentiation take time.
The response is specific because only lymphocytes with complementary receptors are selected. B cells provide the plasma-cell and antibody branch, while T cells provide helper and infected-cell-killing branches. This card stops at the primary effector response; persistent memory and the secondary response are taught separately.
Clonal selection identifies the matching lymphocytes; clonal expansion increases their number. Plasma cells secrete antibodies, whereas T-killer cells kill infected body cells. Do not treat macrophage antigen presentation as antibody production or include memory-cell mechanisms in this primary-response card.
Memory B and T cells make the secondary response faster and stronger
The primary response leaves antigen-specific memory B and T cells in the blood after the infection has been cleared. Their persistence can provide long-term immunity to the same antigen.
- First exposure: the correct lymphocytes are initially scarce, so clonal selection, mitotic expansion and differentiation take time. Plasma cells develop later and begin producing antibodies; symptoms may occur before the response is fully developed.
- Same antigen again: memory cells are already present in larger numbers. They detect the antigen, activate and divide more quickly, producing a faster and stronger secondary response.
- Functional difference: plasma/effector cells act during the immediate response, whereas memory cells persist as a ready population for future exposure. The secondary response produces antibodies more quickly and at a greater concentration, so it may remove the pathogen before symptoms appear.
Primary response → memory B/T cells persist → same antigen is encountered again → matching memory cells activate rapidly → a larger antibody and cellular response removes the pathogen sooner. This memory principle explains how vaccination can provide long-term immunity; vaccine types and vaccination programmes are taught separately.
Memory is specific to the antigen previously encountered, not a general protection against every pathogen. Memory cells are not the same as plasma cells that immediately secrete antibodies, and a faster response does not require invented time, titre or cytokine values.
11.2 Antibodies and Vaccination
- Syllabus
- 9700–2028–2029
- Topic
- 11.2
- Level
- AS
Antibody molecular features connect recognition to immune action
An antibody is a Y-shaped globular glycoprotein secreted by plasma cells. It contains two identical heavy polypeptide chains and two identical light chains held together by disulfide bonds.
| Molecular feature | Functional consequence |
|---|---|
| Variable regions at both tips | Form two identical antigen-binding sites whose shapes are complementary to one antigen epitope, giving specificity |
| Two binding sites | Bind two antigens or particles and can cross-link them into agglutinated groups that phagocytes remove more easily |
| Hinge region | Gives flexibility so both sites can bind epitopes at different orientations or separations |
| Constant region | Binds receptors on immune cells or complement components after antigen binding, promoting opsonisation and other effector responses |
| Disulfide bonds | Stabilise the four-chain Y-shaped molecule while preserving its binding arrangement |
Specific binding forms an antigen–antibody complex. Depending on the target, this can neutralise a toxin or virus, agglutinate cells or pathogens, mark a target for phagocytosis, or activate complement-associated damage.
Variable regions determine antigen specificity; constant regions help recruit later immune effects. Antibodies bind and mark or block targets but do not digest pathogens themselves.
Hybridoma production links antibody specificity to continuous cell division
A hybridoma is a fused cell line used to produce large quantities of one monoclonal antibody. It combines an antibody-producing B-cell lineage with a tumour-cell lineage that can continue dividing.
- Stimulate antibody production: Inject an animal with the relevant antigen so specific antibody-producing B lymphocytes, including plasma-cell descendants, are generated.
- Isolate antibody-producing cells: Remove the stimulated B-cell population from the animal.
- Fuse cell types: Fuse the B cells with tumour cells to form hybridoma cells. The fused cell combines antibody specificity from the B-cell lineage with the capacity for continued mitotic division from the tumour-cell lineage.
- Select and screen: Grow the fusion products in selective medium, then test the surviving hybrid cells for production of the desired antibody. Selection alone does not prove the antibody has the required specificity.
- Clone and expand: Isolate a hybridoma producing the desired antibody, clone that line, and culture it to produce large quantities of identical monoclonal antibody.
The sequence matters: antigen stimulation supplies specificity; fusion supplies a hybrid cell with both antibody production and sustained division; selection removes unsuitable fusion products; screening identifies the required specificity; cloning preserves one antibody-producing cell line for expansion.
This card explains how monoclonal antibodies are made. Their diagnostic and therapeutic uses belong to the next objective; the broader primary immune-response sequence belongs to the neighbouring immune-response card.
Monoclonal specificity enables targeted diagnosis and treatment
All antibodies in one monoclonal preparation have the same binding site, so they bind the same target antigen with high specificity.
| Use | Principle | Meaning of the result |
|---|---|---|
| Diagnosis | Attach a detectable label to a monoclonal antibody; if its target antigen is present in a sample or tissue, binding concentrates the label at that target | A measured signal indicates that the target antigen was bound; controls and a threshold are needed to interpret it |
| Treatment | Choose an antibody that binds an antigen or receptor concentrated on a disease-related cell; binding can block a signal, recruit immune destruction, or deliver an attached drug or radioactive substance to the target | Targeting increases action at antigen-bearing cells, but non-target binding and antigen variation can limit selectivity |
The shared logic is target antigen present → complementary monoclonal antibody binds. Diagnosis converts binding into a detectable signal; treatment converts binding into a local biological or therapeutic effect.
A diagnostic signal shows target binding, not automatically disease severity or complete cause. 'Targeted' treatment is selective rather than perfectly exclusive, so specificity and side effects must still be evaluated.
Active and passive immunity differ in how protection is acquired
Active immunity is protection made by the person’s own immune response after an antigen is encountered. Passive immunity is protection supplied by antibodies made elsewhere, so the recipient’s immune system is not the source of those antibodies.
- Active — natural: Exposure to a pathogen provides the antigen; the person produces antibodies and memory cells. Protection takes time to build, but memory can support a faster, stronger response to the same antigen later.
- Active — artificial: A vaccination provides antigenic stimulation without requiring the person to first develop the disease; the person produces antibodies and memory cells. The specific vaccination process is covered in the following objectives.
- Passive — natural: Ready-made antibodies pass from another person, such as across the placenta or in colostrum. Protection is available without the recipient making the antibodies, but no memory cells are formed.
- Passive — artificial: Ready-made antibodies are injected or infused, for example an antitoxin when rapid protection is needed. Antibodies are available promptly, but the recipient does not form memory cells and may need another antibody supply after reinfection.
The key distinction is who makes the antibodies. Own production in active immunity explains the slower primary response and the presence of memory cells; supplied antibodies in passive immunity explain the immediate protection but the absence of a memory-based secondary response.
Active does not mean immediate, and passive does not create immunological memory. Natural versus artificial describes how the immunity is acquired; active versus passive describes whether the recipient makes the antibodies. This card does not give the detailed steps of vaccination or disease-control programmes.
Vaccination creates active artificial immunity through antigenic memory
A vaccine introduces antigenic material deliberately to produce active artificial immunity. The material is chosen to stimulate a specific immune response without being intended to cause the disease.
- Antigenic stimulation: Vaccine material presents antigens to the immune system. It may contain weakened whole pathogens, inactivated whole pathogens, or selected pathogen components such as proteins, sugars or toxoids.
- Primary response: The antigens trigger a specific immune response, including plasma cells releasing antibodies against the vaccine antigen.
- Memory formation: The response also forms memory cells. These cells preserve the antigen-specific information after the initial response has declined.
- Later exposure: If the person encounters the same antigen again, memory cells help produce a faster and stronger secondary response, so antibodies can rise more rapidly and help control the pathogen before serious disease develops.
Vaccine antigen → primary antibody response → memory-cell formation → quicker, larger secondary response on re-exposure. This is active artificial immunity because the vaccinated person’s own immune system makes the response; the vaccine is not a direct infusion of ready-made antibodies.
A vaccine is not the same as passive antibody treatment, and protection is not an instant guarantee against every exposure. This card explains the immune principle and the safety distinction between vaccine material and disease-causing infection; population vaccination programmes belong to the next objective.
Vaccination programmes reduce transmission as well as individual risk
A vaccination programme protects a population when a sufficiently large proportion of people become immune. This population-level protection is herd immunity: fewer susceptible hosts make it harder for a pathogen to spread.
- Coverage: A coordinated immunisation schedule makes vaccination available across the relevant population. Coverage is not just an individual decision: delivery, access, resources and acceptance affect how many people become immune.
- Fewer susceptible hosts: Each immune person is less likely to contract and pass on the disease, so the pathogen encounters fewer suitable transmission opportunities.
- Transmission falls: When enough people are immune, chains of transmission become harder to maintain and disease levels stay low within the population.
- Indirect protection: People who are not immunised can be less likely to encounter the pathogen because spread is reduced around them. This matters especially for people who cannot rely on vaccination or have higher risk from infection.
- Limits: Herd immunity is not an absolute barrier. If coverage is too low, uneven, inaccessible or poorly maintained, enough susceptible people remain for transmission to continue; protection also depends on the vaccine and pathogen combination rather than on a universal guarantee.
This card is about population coverage and transmission, not the individual vaccine mechanism in 4637 or the active/passive classification in 4636. Herd immunity protects through reduced spread; it does not mean every person is directly vaccinated or that infection is impossible.