Cell recognition and the immune system
AQA
A-Level
Cells carry specific molecules on their cell-surface membrane, mostly proteins or glycoproteins. A protein's highly specific tertiary structure gives it a unique 3D shape, acting as an identity label. The immune system uses these to identify four main targets. First, pathogens (like bacteria) carry foreign antigens. Second, cells from other organisms of the same species carry different antigens, which explains why transplanted tissue or mismatched blood transfusions are attacked. Third, abnormal body cells, such as cancer or virus-infected cells, display altered antigens. Finally, toxins are non-self molecules (not cells) that also stimulate an immune response.
54
Objectives
46
Exam Tips
80
Pitfalls
89
Key Terms
92
Mark Points
Subtopics in this area
Each type of cell has specific molecules on its surface that identify it. These molecules include proteins and enable the immune system to identify: pathogens cells from other organisms of the same species abnormal body cells toxins.
Definition of antigen. The effect of antigen variability on disease and disease prevention.
Phagocytosis of pathogens. The subsequent destruction of ingested pathogens by lysozymes.
The response of T lymphocytes to a foreign antigen (the cellular response).
The role of antigen-presenting cells in the cellular response.
The response of B lymphocytes to a foreign antigen, clonal selection and the release of monoclonal antibodies (the humoral response).
Definition of antibody.
Antibody structure.
The formation of an antigen-antibody complex, leading to the destruction of the antigen, limited to agglutination and phagocytosis of bacterial cells.
The roles of plasma cells and of memory cells in producing primary and secondary immune responses.
The use of vaccines to provide protection for individuals and populations against disease. The concept of herd immunity.
The differences between active and passive immunity.
Structure of the human immunodeficiency virus (HIV) and its replication in helper T cells.
How HIV causes the symptoms of AIDS. Why antibiotics are ineffective against viruses.
The use of monoclonal antibodies in: targeting medication to specific cell types by attaching a therapeutic drug to an antibody medical diagnosis.
Ethical issues associated with the use of vaccines and monoclonal antibodies.
The use of antibodies in the ELISA test.
Students should be able to: discuss ethical issues associated with the use of vaccines and monoclonal antibodies evaluate methodology, evidence and data relating to the use of vaccines and monoclonal antibodies.
Cell recognition and the immune system Revision Guide
Learning Objectives
What you need to know and understand
- Name the four categories of material the immune system identifies as foreign.
- Explain how the tertiary structure of a surface protein allows a lymphocyte to distinguish a self cell from a non-self cell.
- Suggest why tissue transplanted from another person is attacked while the patient's own tissue is not.
- State in one sentence what an antigen is, naming the type of molecule, where it is found and what it does.
- Explain, as an unbroken chain from mutation to symptoms, why a person can catch influenza repeatedly.
- Suggest why a vaccine effective against one strain of a pathogen may give no protection against another strain of the same species.
- Describe phagocytosis as a sequence of distinct stages, naming the vesicle and the organelle involved.
- Explain what happens to the products of hydrolysis inside a phagocyte.
- Distinguish the non-specific action of a phagocyte from the specific response of a lymphocyte.
- Describe the cellular response as a sequence from antigen presentation to the differentiation of the clone.
- Explain how a cytotoxic T cell destroys a virus-infected cell, naming perforin and its effect on the cell-surface membrane.
- Suggest why cells carrying a mutated membrane protein, such as those in a tumour, can be destroyed by the immune system.
- Identify three different cells that can act as antigen-presenting cells and state how each acquires the antigen it displays.
- Explain why antigen presentation speeds up the cellular response, using the idea of one specific receptor per T cell.
- Describe what happens to a helper T cell immediately after it binds to a presented antigen.
- Describe the humoral response from antigen binding to antibody secretion, using the terms clonal selection and clonal expansion correctly.
- Explain why the antibodies released by one clone of plasma cells are all identical.
- Explain the role of the helper T cell in activating a B cell, and predict what would happen to antibody production if helper T cells were destroyed.
- State the definition of an antibody in one sentence containing all four creditworthy elements.
- Explain why a given antibody binds only one antigen, referring to tertiary structure and complementary shape.
- Identify and correct an answer that describes antibody binding using enzyme vocabulary such as active site or induced fit.
- Draw and label an antibody, marking the variable regions, constant region, hinge region and disulfide bridges.
- Explain how the variable region gives an antibody its specificity, referring to amino acid sequence and tertiary structure.
- Explain how having two binding sites and a flexible hinge makes agglutination possible.
- Describe how an antigen-antibody complex forms and explain why binding is specific.
- Explain how agglutination increases the rate at which bacteria are destroyed by phagocytes.
- Describe the destruction of bacterial cells by agglutination and phagocytosis, as limited by the specification.
- Describe three measurable differences between a primary and a secondary response using an antibody concentration graph.
- Explain why the primary response has a lag of several days before antibody appears.
- Explain the different roles of plasma cells and memory cells, stating the lifespan of each.
- Explain how a vaccine produces long-term protection without the person developing the disease.
- Explain herd immunity in terms of transmission, and identify who it protects.
- Suggest what happens to the incidence of a disease in a population when vaccination coverage falls below the threshold.
- Contrast active and passive immunity in paired statements covering antigen exposure, memory cells, speed and duration.
- Classify examples such as vaccination, infection, breast milk and antivenom as active or passive, natural or artificial.
- Explain why passive immunity gives immediate but temporary protection.
- Label the structure of HIV from the RNA core outwards, naming the enzyme it carries.
- Describe HIV replication in a helper T cell as a series of ordered steps.
- Explain why a drug that inhibits reverse transcriptase would slow HIV replication but not affect the host cell's own transcription.
- Explain the chain of events from the loss of helper T cells to the appearance of AIDS symptoms.
- State two pieces of evidence a doctor needs before diagnosing AIDS, and explain why an antibody test alone is insufficient.
- Give a named bacterial structure or process targeted by antibiotics and explain why its absence makes viruses unaffected.
- Explain how attaching a drug to a monoclonal antibody reduces the dose needed and the side effects experienced.
- Describe how a labelled monoclonal antibody is used to detect the presence of a specific antigen.
- Suggest a reason why a targeted antibody therapy might still damage some healthy cells.
- Identify three distinct ethical issues raised by the use of vaccines and three raised by the use of monoclonal antibodies.
- Explain why a control group in a cancer drug trial is given an existing treatment rather than a placebo.
- Construct a balanced argument, for and against, about a named use of a vaccine or monoclonal antibody, and justify a conclusion.
- Describe the ELISA procedure in order, naming what binds at each stage and stating the purpose of every washing step.
- Explain why a positive ELISA result in a baby born to an HIV-positive mother is not proof of infection.
- Evaluate an antibody-based diagnostic test against alternatives using data on detection rate and time after the onset of symptoms.
- Discuss the ethical issues surrounding the development and use of vaccines and monoclonal antibodies, including animal testing and clinical trial risks.
- Evaluate methodology and data from vaccine and mAb studies by identifying limitations such as sample size, study duration, and lack of controls.
- Interpret standard deviations and error bars correctly, understanding their relationship to statistical significance without overgeneralising.
Marking Points
Key points examiners look for in your answers
- One mark for identifying the molecules as proteins or glycoproteins in the cell-surface membrane, each with a specific tertiary structure.
- One mark for identifying pathogens as a source of foreign antigens.
- One mark for identifying cells from other organisms of the same species, such as transplanted tissue or mismatched blood.
- One mark for identifying abnormal body cells, with cancer cells or virus-infected cells accepted as named examples.
- One mark for identifying toxins as non-self molecules that stimulate an immune response.
- one mark for defining an antigen as a molecule, usually a protein or glycoprotein, recognised as foreign or non-self, that stimulates an immune response
- one mark for mutation changing the base sequence and therefore the amino acid sequence of the antigen
- one mark for the changed tertiary structure no longer being complementary to existing antibodies or memory cell receptors
- one mark for the consequence that memory cells cannot bind, so a primary response occurs again and symptoms appear
- one mark for applying this to prevention, such as an influenza vaccine having to be changed each year
- The phagocyte is attracted to the pathogen by chemical products and binds to antigens on the pathogen surface.
- The pathogen is engulfed by endocytosis to form a vesicle known as a phagosome.
- Lysosomes migrate towards and fuse with the phagosome.
- Lysozymes are released into the phagosome and destroy the ingested pathogen by hydrolysis.
- The phagocyte displays the pathogen's antigens on its own cell-surface membrane to become an antigen-presenting cell.
- one mark for a foreign or faulty protein being recognised as an antigen on an antigen-presenting cell
- one mark for a specific T cell with a complementary receptor binding to the presented antigen
- one mark for the activated T cell dividing by mitosis to form a clone (clonal expansion)
- one mark for helper T cells releasing cytokines that stimulate phagocytes and B cell division
- one mark for cytotoxic T cells releasing perforin to make the infected cell's membrane freely permeable
- Define an antigen-presenting cell as a cell displaying antigen on its cell-surface membrane, and note that the displayed antigen may be foreign or an abnormal self-antigen.
- Name at least two sources and state how each acquires its antigen: a phagocyte after hydrolysing a pathogen, a virus-infected body cell, or a B cell that has taken in antigen by endocytosis.
- State that a T cell with a complementary receptor binds to the presented antigen.
- Explain that presentation increases the chance of a lymphocyte meeting its specific antigen, because each T cell recognises only one antigen and such cells are rare.
- State that the activated helper T cell divides by mitosis to form a clone.
- Distinguish transplanted cells, which present foreign donor antigens, from cancer cells, which present abnormal self-antigens.
- Antigen binds to the complementary antibody or receptor on one specific B cell; this is clonal selection.
- B cell processes and presents the antigen and is activated by cytokines from a helper T cell.
- Clonal expansion follows: division by mitosis to produce a clone of identical cells.
- Plasma cells secrete antibodies that are identical, or monoclonal, and specific to that antigen.
- The remainder of the clone differentiates into memory B cells.
- Distinguish clonal selection (antigen binding to the specific B cell) from clonal expansion (mitotic division of that activated cell).
- An antibody is a protein or immunoglobulin with a quaternary structure.
- It is secreted by plasma cells derived from B lymphocytes.
- It is produced in response to a specific foreign antigen.
- The binding site has a tertiary structure complementary to that antigen, forming an antigen-antibody complex.
- Distinguish membrane-bound antibody on a B cell from secreted antibody released by a plasma cell.
- The antibody has four polypeptide chains, two heavy and two light, giving it a quaternary structure.
- Disulfide bridges hold the polypeptide chains together.
- Two variable regions form two binding sites with a tertiary structure complementary to one specific antigen.
- The constant region is the same in all antibodies of a specific class and binds to receptors on phagocytes.
- The hinge region provides flexibility so that two separate antigens or pathogens can be bound simultaneously.
- one mark for the antibody binding site being complementary to the antigen, so an antigen-antibody complex forms
- one mark for each antibody having two binding sites, so one antibody binds antigens on two different bacterial cells
- one mark for agglutination, described as the clumping together of bacteria by antibodies
- one mark for phagocytes engulfing the clump, so many bacteria are destroyed at once
- one mark for explaining why clumping helps: one phagocyte can engulf many bacteria, and the bacteria cannot spread as easily
- one mark for the primary response being slow because few lymphocytes have a complementary receptor and clonal selection and division take time
- one mark for plasma cells secreting antibody and being short-lived
- one mark for memory cells remaining in the blood for years without secreting antibody
- one mark for memory B cells dividing rapidly into plasma cells on second exposure to the same antigen
- one mark for the secondary response producing antibody faster, at a higher concentration and for longer, so symptoms do not appear
- one mark for the vaccine containing antigens, from a dead or attenuated pathogen or as an isolated antigen
- one mark for a primary response producing memory cells without the person developing the disease
- one mark for memory cells producing a faster secondary response with a higher concentration of antibody on later exposure
- one mark for herd immunity described as a large enough proportion of the population being immune or vaccinated
- one mark for unvaccinated people being protected because the pathogen is less likely to be transmitted to them
- one mark for active immunity involving exposure to antigen and the person's own production of antibody
- one mark for passive immunity involving antibodies introduced from outside, with the person's own immune system not producing them
- one mark for active immunity producing memory cells whereas passive immunity does not
- one mark for the contrast in timing: passive protection is immediate but short-lived, active protection is slower to develop but long-lasting
- one mark for a valid example on each side, such as vaccination and an anti-toxin injection or maternal antibodies
- Attachment proteins on the virus bind to specific receptors (CD4) on the helper T cell.
- The viral lipid envelope fuses with the cell-surface membrane, releasing viral RNA and enzymes into the cell.
- Reverse transcriptase synthesises a complementary DNA strand from the viral RNA template.
- The newly formed viral DNA is inserted into the host cell's DNA.
- Host cell ribosomes are used to translate viral mRNA into viral proteins (e.g., capsid proteins or enzymes).
- New viruses are assembled and released by budding, acquiring their lipid envelope from the host cell membrane.
- State that HIV replication destroys helper T cells, leading to a significant fall in their numbers.
- Explain that fewer helper T cells means reduced activation of B cells and cytotoxic T cells, resulting in decreased antibody production.
- Attribute the symptoms of AIDS to secondary or opportunistic infections rather than the direct action of HIV.
- Note that diagnosis of AIDS requires a low helper T cell (CD4) count or an AIDS-defining illness, not simply the presence of antibodies.
- Clarify that antibiotics are ineffective against viruses because viruses lack bacterial structures or metabolic processes, such as a murein cell wall or ribosomes, for the drugs to target.
- one mark for monoclonal antibodies being identical, and specific to one antigen, because they come from one clone of cells
- one mark for the binding site being complementary to an antigen found on, or in greater numbers on, the target cells
- one mark for the drug being attached to the antibody and so delivered to those cells, with an antigen-antibody complex forming
- one mark for the consequence, that a lower dose can be used and there are fewer side effects on healthy cells
- one mark for the antibody carrying an enzyme, dye or radioactive label in a diagnostic test, so the antigen can be located or measured
- one mark for identifying a specific ethical issue, such as the use of animals in producing or testing the treatment
- one mark for the point that it is not ethical to withhold an effective treatment, so a control group receives an existing drug rather than a placebo if a treatment already exists
- one mark for a risk-benefit argument, such as rare side effects in individuals set against protection of the population
- one mark for an issue of consent, autonomy or fair distribution, such as compulsory vaccination or limited vaccine supply
- one mark for reaching a justified conclusion that refers to the context in the question
- one mark for an antibody with a binding site complementary to the antigen binding to it, forming an antigen-antibody complex
- one mark for a second or labelled antibody, with an enzyme attached, binding to that complex
- one mark for washing to remove unbound antibody, since otherwise a colour change gives a false positive
- one mark for the enzyme acting on an added substrate to produce a colour change, with the intensity of colour proportional to the quantity present
- one mark for interpreting a positive result with care, for example maternal antibodies crossing the placenta producing a positive result in an uninfected baby
- Identify specific methodological limitations in vaccine or mAb trials, such as small sample sizes, lack of a control group, or short study duration.
- State that overlapping standard deviations indicate differences may not be significant, but a statistical test is needed to confirm if differences are due to chance.
- Discuss ethical concerns of vaccines, such as the use of animals in development, side effects, or the balance between individual risk and herd immunity.
- Explain ethical issues with monoclonal antibodies, including the use of mice to produce B cells (e.g., injecting mice with antigens) or the risks associated with early human clinical trials.
Examiner Tips
Expert advice for maximising your marks
- 💡Check whether the question asks for molecules or for cells; 'give two types of cell' has a different acceptable list from 'give two examples of antigens'.
- 💡Use the four specification categories by name rather than vague phrases such as 'foreign things'.
- 💡Learn the definition as a single sentence containing three elements: type of molecule, recognised as foreign, stimulates an immune response.
- 💡Finish the whole chain in variability questions: mutation, different amino acid sequence, different tertiary structure, not complementary, no secondary response, symptoms.
- 💡Write 'not complementary' rather than 'does not fit'; the complementary-shape wording is what mark schemes look for.
- 💡Work through the distinct stages logically: attract, bind, engulf, fuse, hydrolyse, and present. Ensure you name both the phagosome and lysosome.
- 💡Avoid using osmosis or diffusion vocabulary; marks are awarded for specific terms like endocytosis and hydrolysis.
- 💡Always use 'complementary' when describing the fit between the T cell receptor and the antigen; 'same shape' will not be credited.
- 💡When asked how the immune system destroys abnormal cells, start by stating that the abnormal protein is recognised as a foreign antigen.
- 💡Finish an 'explain the role' answer with the consequence, activation of the T cell and clonal expansion, not just with the display of antigen.
- 💡When asked to give cell types that stimulate an immune response, antigen-presenting cells such as macrophages and infected body cells are valid examples; check the wording of the question before committing.
- 💡Always specify that plasma cells secrete antibodies; do not state that memory cells or T cells produce them.
- 💡Use sequencing verbs (binds, presents, is activated, divides, differentiates, secretes) so the order of events is unambiguous.
- 💡Write the definition as four distinct clauses (protein, plasma cell origin, specific antigen trigger, complementary binding site) to ensure completeness.
- 💡Never import enzyme vocabulary; antibodies have binding sites, not active sites, and they do not show induced fit.
- 💡Label a sketch with variable region, binding site, constant region, hinge region, and disulfide bridge to clearly demonstrate structural knowledge.
- 💡Pair every structural feature with its function, such as linking the presence of two binding sites to the ability to cause agglutination.
- 💡Two binding sites is the sentence that makes agglutination work; include it every time.
- 💡Say why clumping helps, one phagocyte engulfs many bacteria, rather than leaving the examiner to infer it.
- 💡Stick to agglutination and phagocytosis of bacterial cells; the specification limits destruction of the antigen to these two mechanisms.
- 💡Graph questions want three comparisons every time: faster, higher, and lasting longer. Quote figures from both axes.
- 💡If the second exposure is to a different pathogen, say so and explain that a primary response happens again.
- 💡Name the cell doing each job; 'the immune system responds faster' scores nothing without plasma cells and memory cells.
- 💡When asked how vaccination protects a population as well as an individual, write the two explanations separately; the population mark is for interrupted transmission.
- 💡Name who benefits from herd immunity, for example babies too young to be vaccinated or immunocompromised patients, to earn the application mark.
- 💡Use 'proportion' or 'percentage' of the population rather than 'lots of people'.
- 💡Contrast questions need paired statements in one sentence: active produces memory cells whereas passive does not.
- 💡Draft a two-column table in rough, source of antibody, speed, duration, memory cells, then turn each row into one comparative sentence.
- 💡In data questions on anti-toxin treatment, name the group who should receive it and support the choice with a figure.
- 💡When describing viral replication, structure your answer chronologically: attachment, entry, reverse transcription, integration, protein synthesis, assembly, and release.
- 💡Always name 'reverse transcriptase' when discussing HIV replication; this specific enzyme distinguishes retroviruses from other viral replication cycles.
- 💡If asked to label an HIV diagram, ensure you correctly identify the attachment proteins on the exterior and the RNA and reverse transcriptase within the core.
- 💡When asked why antibiotics are ineffective against viruses, always name a specific bacterial target the virus lacks, such as a murein cell wall or metabolic enzymes.
- 💡Open an AIDS pathogenesis answer by attributing the symptoms to secondary infections, then explain the underlying fall in helper T cells that prevents antibody production.
- 💡If a question asks what else is needed to diagnose AIDS, give a low helper T cell count or an AIDS-defining illness, not just an antibody test.
- 💡Answer in three moves: the antibody is specific to an antigen on the target cell, the drug is attached to the antibody, so only target cells receive the drug.
- 💡In diagnosis questions name the label and say what makes it visible, colour change, fluorescence or radioactivity.
- 💡Use data from the stem about antigen numbers rather than asserting that only diseased cells carry the antigen.
- 💡Anchor every point in the context: name the disease, the treatment and the people affected.
- 💡If the command word is discuss, give at least one point on each side and then a conclusion.
- 💡Where a trial has no placebo group, say explicitly that withholding an effective treatment from ill patients would be unethical.
- 💡Track each molecule through the diagram in order and name it: antigen, first antibody, second antibody with enzyme, substrate, colour change.
- 💡In 'evaluate this test' questions use the data first, how early the disease is detected and how many positives are found, before commenting on speed, cost and access to laboratories.
- 💡Do not confuse ELISA with lateral flow (immunochromatography) tests: ELISA is performed in wells of a microtitre plate, whereas a lateral flow test uses a test strip with a control line to show the sample has moved along the strip.
- 💡When evaluating data, always quote specific figures from the provided tables or graphs to support your arguments.
- 💡If asked to discuss ethics, ensure you mention both the benefits (e.g., herd immunity, targeted cancer treatment) and the drawbacks (e.g., animal testing, side effects).
Common Mistakes
Pitfalls to avoid in your exam answers
- Answering 'toxins' when the question asks for types of cell. Correction: A toxin is a molecule, not a cell; read the question carefully.
- Offering 'B cells' or 'T cells'. Correction: These are the cells that respond to the antigen, not the foreign cells being recognised.
- Writing 'the immune system recognises the cell' without naming the antigen. Correction: Always specify that the immune system recognises the specific antigen or surface protein.
- defining an antigen as 'a pathogen' or 'a germ' rather than as a molecule carried by the pathogen
- writing that the pathogen changes its antibodies; pathogens carry antigens and only plasma cells make antibodies
- placing the mutation in the infected person rather than in the pathogen
- claiming antigen variability destroys memory cells, when the memory cells still exist but are no longer complementary
- saying 'the vaccine stops working' without explaining the loss of complementary shape
- Confusing the lysosome with lysozyme. Correction: The lysosome is the organelle (vesicle); lysozyme is the hydrolytic enzyme it releases.
- Stating that the pathogen is 'absorbed' or 'dissolved'. Correction: Correctly state it is hydrolysed or destroyed by lysozymes.
- Describing phagocytosis as a specific response. Correction: It is a non-specific immune response that targets any pathogen, unlike the specific lymphocyte response.
- stating that T cells produce antibodies; only plasma cells derived from B cells secrete antibodies
- claiming that helper T cells stimulate clonal selection of B cells; antigens cause selection, while helper T cells stimulate clonal expansion
- stating that cytotoxic T cells 'kill the cell' without a mechanism; you must specify that perforin makes the membrane freely permeable
- Assuming only phagocytes present antigens, and so losing the marks for infected body cells and B cells. Correction: name at least two sources and state how each acquires its antigen.
- Saying the antigen-presenting cell 'gives' the antigen to the T cell rather than displaying it for binding. Correction: the antigen is displayed on the membrane and the T cell's receptor binds to it.
- Confusing antigen presentation with antibody production. Correction: presentation is display of antigen; antibody production is secretion by plasma cells.
- Describing antigen-presenting cells as a type of lymphocyte. Correction: macrophages and infected body cells are not lymphocytes, though B cells are.
- Describing the display of antigen but never stating the advantage it brings, which is where the explain mark sits. Correction: finish with the increased probability of a complementary T cell meeting the antigen.
- Stating that transplanted cells display their own abnormal antigens. Correction: transplanted cells carry foreign donor antigens, whereas cancer cells display abnormal self-antigens.
- Saying the B cell makes a new antibody to fit the antigen; the antibody already exists and the antigen selects the cell that makes it. Correction: the antigen selects a pre-existing complementary B cell.
- Using clonal selection and clonal expansion interchangeably; selection is antigen binding to the specific B cell, expansion is division. Correction: keep the two terms for the two distinct events.
- Writing that B cells divide by meiosis; they divide by mitosis to produce genetically identical clones. Correction: mitosis produces identical plasma and memory cells.
- Stating that memory B cells secrete antibodies; only plasma cells secrete antibodies. Correction: memory B cells remain in circulation and respond rapidly on re-exposure.
- Attributing clonal selection to helper T-cell activation. Correction: clonal selection is antigen binding to the B cell; helper cytokines drive clonal expansion.
- Calling the antibody's binding site an active site; antibodies are not enzymes and have binding sites. Correction: use 'binding site' and avoid enzyme vocabulary.
- Saying antibodies kill or destroy pathogens directly; they bind to antigens and mark them for destruction. Correction: binding leads to agglutination, neutralisation or enhanced phagocytosis.
- Swapping antigen and antibody within one sentence, which reverses the biological meaning. Correction: the antigen is the foreign molecule; the antibody is the protein that binds it.
- Attributing antibody production to T cells or to phagocytes. Correction: plasma cells derived from B lymphocytes secrete antibodies.
- Stating that B lymphocytes secrete antibodies. Correction: B cells carry membrane-bound antibody; plasma cells secrete antibody.
- Labelling the binding site as an active site; antibodies are not enzymes.
- Claiming the antibody changes shape to fit the antigen; antibodies do not show induced fit.
- Saying the variable region is the same in all antibodies; it is the constant region that is conserved within a class.
- Drawing a single binding site, which makes explaining agglutination impossible.
- saying the antibody dissolves, digests or kills the bacterium itself; antibodies do not destroy bacteria directly, phagocytes do
- describing agglutination as antibodies sticking to each other rather than binding antigens on separate cells
- explaining agglutination and then stopping, when the specification pairs it with phagocytosis of the clumped bacteria
- writing 'the antibody destroys the antigen' with no mechanism at all
- forgetting that an antibody with only one binding site could not clump anything, because cross-linking needs two
- saying memory cells produce antibodies; they divide into plasma cells, which do
- describing secondary antibodies as stronger or better, when the antibody is identical and only the speed and quantity change
- reading an antibody concentration graph and commenting on the peak but not the time lag
- assuming memory cells protect against any pathogen, when they are specific to one antigen
- using 'immune' to mean the pathogen cannot enter the body, when it enters but is destroyed before symptoms appear
- writing that a vaccine contains antibodies; it contains antigens and produces active immunity
- saying vaccination makes a person immune immediately, when the primary response takes days
- explaining herd immunity as unvaccinated people somehow catching immunity from vaccinated people
- claiming everyone must be vaccinated, when herd immunity needs a sufficiently large proportion, not all
- confusing attenuated, meaning weakened but alive, with dead
- answering a 'contrast' question with facts about only one type; the contrast command word requires both sides of each difference
- saying passive immunity lasts until the antigens are gone, when it ends as the introduced antibodies are broken down
- treating antibodies in breast milk as active immunity for the baby
- claiming passive immunity produces memory cells simply because antibodies are present
- assuming active immunity is always natural and passive immunity always artificial; both can be natural or artificial
- Calling the virus's attachment protein a receptor; correction: receptors are located on the host cell membrane, whereas the virus possesses attachment proteins.
- Stating that HIV contains DNA or replicates by mitosis; correction: HIV is an RNA retrovirus that relies entirely on host cell machinery to replicate, not cell division.
- Saying the virus makes its own proteins; correction: viruses lack ribosomes, so they must use the host cell's ribosomes for translation.
- Describing HIV as replicating in B cells; correction: HIV specifically targets and replicates within helper T cells.
- Stating HIV causes the symptoms of AIDS directly, instead of through infections the weakened immune system cannot fight. Correction: Attribute symptoms to opportunistic secondary infections.
- Writing that antibiotics cannot get inside the virus, rather than that viruses lack the bacterial structures and metabolic processes antibiotics disrupt. Correction: Name a bacterial target such as the murein cell wall or ribosomes that viruses lack.
- Confusing antibiotic resistance with immunity; bacteria become resistant, they do not become immune. Correction: Use 'resistant' for bacteria and 'immune' for the host.
- Treating a positive HIV antibody test as proof that a person has AIDS. Correction: State that AIDS requires a low CD4 count or an AIDS-defining illness.
- saying the antibody kills the cancer cell, when the attached drug does so after the antibody has bound
- claiming the target antigen is found only on cancer cells, when it is usually present in far greater numbers there
- describing the binding as an active site or as an enzyme-substrate reaction
- leaving out why side effects are reduced, which is a key part of explaining the advantage of targeted medication
- using the word monoclonal without saying that all the molecules are identical
- writing personal opinion with no biological reasoning behind it
- stating 'it is wrong to test on animals' without saying what the testing is for or what the alternative would be
- offering practical or economic points, such as storage temperature, as ethical issues
- arguing only one side when the question expects a judgement to be justified
- claiming that a placebo is always used in a drug trial, forgetting that an existing treatment is used as a control if withholding it would be unethical
- describing the antigen-antibody binding as an enzyme-substrate reaction; only the attached label is an enzyme
- omitting the washing steps, which carry marks in their own right
- treating a positive result as proof of current infection, when antibodies persist after infection and can be maternal
- confusing which molecule is fixed to the well; in the HIV test the antigen is fixed and the patient supplies the antibody
- saying the colour only shows presence, when the depth of colour gives a quantitative result
- Stating that overlapping error bars definitively prove there is no significant difference. Correction: State that overlap suggests the difference might not be significant, but a statistical test is required for proof.
- Ignoring ethical issues regarding animal use in mAb production. Correction: Explicitly mention that producing mAbs often involves injecting mice with antigens, raising animal welfare concerns.
- Providing a one-sided evaluation of vaccine data. Correction: Always evaluate both supporting and conflicting evidence when assessing data on vaccine efficacy or safety.