11. Immunity

Phagocytes are white blood cells that provide an early, non-specific immune response by carrying out phagocytosis: they attach to a pathogen, engulf it and digest it.

1. Chemicals from pathogens and attacked body cells attract a phagocyte; movement towards the stimulus is chemotaxis.
2. Receptor proteins on the phagocyte attach to antigens on the pathogen.
3. The cell-surface membrane extends around the pathogen and encloses it in a phagocytic vacuole, or phagosome; this is endocytosis.
4. The phagosome fuses with a lysosome to form a phagolysosome. Lysosomal digestive enzymes enter the vacuole and destroy the pathogen.

Neutrophils are short-lived phagocytes that patrol tissues and are released in large numbers during infection. Macrophages are longer-lived, settle in organs and carry out phagocytosis without completely destroying the pathogen: they display pathogen antigens on their surface as antigen-presenting cells, allowing lymphocytes to recognise them.

Phagocytosis is a non-specific early defence, not antibody production. Neutrophils digest pathogens completely and then die; macrophages have the additional antigen-presentation role that links phagocytosis to later specific immunity. The detailed primary response and memory-cell sequence belong to later cards.

An antigen is a molecular marker on a cell or pathogen surface that allows cell-to-cell recognition. The immune system uses the distinction between self and non-self antigens to decide whether an immune response is stimulated.

• Human body cells carry surface markers that identify them as part of the body.
• Bacteria and viruses carry their own surface markers; antigens can be found on bacterial cell walls or on virus surfaces.
• Some glycolipids and glycoproteins on the outer surface of cell-surface membranes act as antigens.

• Self antigen: produced by the organism’s own body cells; it normally does not stimulate an immune response.
• Non-self antigen: not produced by the organism’s own body cells, including antigens on pathogenic bacteria and viruses; it stimulates an immune response.

An antigen is a recognised surface marker, not necessarily the whole pathogen. Antigen recognition provides the signal for later specific immune responses; the detailed lymphocyte receptor matching, primary-response sequence and memory-cell mechanism belong to the following cards.

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.

1. A macrophage presents pathogen antigen fragments; antigens may also be displayed on a pathogen or an infected body cell.
2. The B- and T-lymphocytes with receptors complementary to the antigen are selected. This is clonal selection.
3. The selected lymphocytes divide by mitosis, producing many clones with the same antigen specificity. This is clonal expansion.
4. 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.
5. 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.

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.

An antibody is a Y-shaped globular glycoprotein produced by B lymphocytes, including plasma cells. Its two heavy and two light polypeptide chains are joined by disulfide bonds; variable regions at the tips form antigen-binding sites.

• Variable region → specificity: the binding site is complementary to a region of an antigen called an epitope, so an antibody binds its matching antigen and forms an antigen–antibody complex.
• Hinge → flexibility: movement at the hinge helps the binding sites approach antigens at different angles.
• Constant region → effector action: after binding, the antibody can block a virus entering cells or neutralise a toxin; it can also make bacteria easier for phagocytes to recognise (opsonisation), clump pathogens together (agglutination), or contribute to lysis, including complement-associated lysis.

The same recognition logic links binding to different outcomes: specific antigen attachment blocks or neutralises a target directly, or marks/organises pathogens so phagocytes can engulf them; complement-associated action can contribute to pathogen lysis.

Variable regions determine which antigen is bound; the constant region helps determine what happens after binding. Antibodies do not digest pathogens themselves. The primary-response production sequence belongs to 4631, while hybridoma production, monoclonal uses, immunity types and vaccines belong to 4634–4638.

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.

1. Stimulate antibody production: Inject an animal with the relevant antigen so specific antibody-producing B lymphocytes, including plasma-cell descendants, are generated.
2. Isolate antibody-producing cells: Remove the stimulated B-cell population from the animal.
3. 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.
4. 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.
5. 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.

A monoclonal antibody binds one target antigen with high specificity. That selective binding can reveal where the target is, or attach an intervention to cells or molecules carrying the target.

• Diagnostic detection: A monoclonal antibody can bind a pathogen antigen or a marker on a cancer cell. A visible or measurable label on the antibody then reveals whether the target is present; examples include tests for HIV, detection of bacterial pathogens, distinguishing related viruses, and locating blood clots by labelled antibody binding to fibrin.
• Targeted treatment: A monoclonal antibody can bind a chosen cell-surface protein or inflammatory target, so the associated immune or therapeutic effect is focused on cells or processes carrying that target. SME-supported examples include treatment directed at cancer cells, reducing an inflammatory response, and supplying purified antibodies against rabies virus.
• Other selective uses: The same binding principle supports research or separation work when a particular antigen must be captured or identified rather than all surrounding molecules.

Specificity is the control point: target antigen present → monoclonal antibody binds → the attached label makes the target detectable, or the attached/triggered action changes the target-bearing cell or process. The method is selective because unrelated antigens are not the intended binding target.

This card covers what monoclonal-antibody specificity enables. Antibody structure and general effector functions belong to 4633; hybridoma production belongs to 4634; immunity types and vaccination belong to the later objectives. A diagnostic signal shows target binding, not automatically the severity or complete cause of disease.

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.

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.

1. 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.
2. Primary response: The antigens trigger a specific immune response, including plasma cells releasing antibodies against the vaccine antigen.
3. Memory formation: The response also forms memory cells. These cells preserve the antigen-specific information after the initial response has declined.
4. 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.

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.