amazon.co.ukImmunity
A-Level Biology revision on immunity: non-specific defences, phagocytosis, cell-mediated and humoral responses, antibodies, vaccination, herd immunity, monoclonal antibodies and HIV, with multi-board exam practice and mark-scheme logic.
🎯 Learning Objectives
- Describe non-specific defences (barriers, inflammation, phagocytosis) and antigen presentation (AQA 3.2.4; OCR 4.1.1)
- Describe cell-mediated immunity: T-helper and T-cytotoxic cells and clonal selection/expansion (AQA 3.2.4; OCR 4.1.1)
- Describe humoral immunity: B cells, plasma cells, antibody structure and action (AQA 3.2.4; OCR 4.1.1)
- Compare primary and secondary responses and explain vaccination and herd immunity (AQA 3.2.4; Edexcel A T6)
- Distinguish active and passive immunity and describe monoclonal antibody uses (ELISA, pregnancy tests, targeted therapy)
- Describe HIV structure and replication and explain antibiotic action and resistance (AQA 3.2.4/3.8; OCR 4.1.1)
📋 Key Definitions and Core Concepts
Pathogen: A disease-causing microorganism (bacterium, virus, fungus, protoctist) that triggers an immune response.
Antigen: A cell-surface molecule (usually a glycoprotein or glycolipid) that the immune system recognises as foreign (non-self), triggering an immune response.
Phagocytosis: Non-specific engulfment of pathogens by phagocytes: the pathogen is enclosed in a phagosome that fuses with lysosomes so hydrolytic enzymes digest it; the phagocyte then presents the antigens.
Antigen-presenting cell (APC): A phagocyte (or infected body cell) that displays foreign antigens on its cell-surface membrane after digesting a pathogen, activating specific T cells.
Clonal selection and expansion: The process by which a specific complementary B or T cell is selected by an antigen, then stimulated to divide by mitosis into many genetically identical cells (a clone).
Plasma cell: A B cell differentiated during the primary response that secretes large quantities of specific antibodies; short-lived.
Memory cell: A long-lived B or T cell formed in the primary response that remains in the blood; on re-exposure it enables a faster, stronger secondary response.
Antibody: A Y-shaped protein (immunoglobulin) of two heavy and two light polypeptide chains joined by disulfide bridges; variable regions form complementary antigen-binding sites, the constant region binds phagocytes.
Herd immunity: When a sufficiently high proportion of a population is vaccinated (or immune) that pathogens cannot spread easily, protecting unvaccinated individuals.
Active immunity: Immunity from the production of antibodies by the person's own immune system after exposure to an antigen (natural infection or vaccination); slow but long-lasting with memory cells.
📌 Key Points
Non-specific: skin, mucus, lysozyme, inflammation; phagocytosis: chemotaxis → phagosome → lysosome fusion → hydrolysis → antigen presentation
Cell-mediated: APC activates complementary T-helper cells → clonal expansion → T-cytotoxic cells kill infected/tumour cells with perforin
Humoral: T-helper activates B cells → clonal expansion → plasma cells (antibodies) + memory B cells
Antibody: 2 heavy + 2 light chains, disulfide bridges; variable region complementary to antigen; forms antigen-antibody complex; agglutination/opsonisation
Primary response: slow (clonal selection), antibody rises then falls; secondary: faster, stronger, longer (memory cells)
Vaccines: weakened/inactivated pathogens or antigens → active immunity; herd immunity protects the unvaccinated
HIV: RNA + reverse transcriptase in capsid; infects T-helper cells; reverse transcription → DNA → host transcription → viral proteins → budding
Antibiotics: target bacterial structures (cell wall, ribosomes); resistance via mutation + selection pressure
Non-specific defences and phagocytosis (AQA 3.2.4; OCR 4.1.1)
The body's first lines of defence are non-specific - they respond to any pathogen the same way. Physical barriers: the skin (keratinised, impermeable, flora outcompete pathogens), mucus in the airways (secreted by goblet cells, traps pathogens, moved by cilia), lysozyme in tears and saliva (hydrolyses bacterial cell walls), stomach acid (pH ~2 kills most ingested pathogens), and blood clotting sealing wounds. Inflammation at a wound: histamine release from mast cells causes vasodilation (redness, heat) and increased capillary permeability (swelling), bringing phagocytes and plasma proteins to the site.
Phagocytosis is the key non-specific cellular defence and a guaranteed sequence question (from the existing site content): (1) phagocytes (e.g. macrophages, neutrophils) are attracted to pathogens by chemicals they release (chemotaxis); (2) the phagocyte extends its cell-surface membrane around the pathogen, engulfing it into a phagosome; (3) lysosomes fuse with the phagosome, releasing hydrolytic enzymes (e.g. lysozyme) that digest the pathogen; (4) soluble products are absorbed into the cytoplasm; (5) the phagocyte becomes an antigen-presenting cell (APC), displaying the pathogen's antigens on its cell-surface membrane. Antigen presentation is the bridge to the specific immune response: these antigens stimulate complementary T-helper cells, which in turn activate specific B cells. When answering, always link the non-specific phase to the specific phase through the APC - that connection is where most marks are lost.
Inflammation deserves the detail the mark schemes list: damaged tissues and mast cells release histamine, which causes arterioles to vasodilate (redness, heat) and capillaries to become more permeable (swelling, oedema), delivering plasma proteins and phagocytes to the infection; the increased blood flow raises the local temperature, slowing pathogen reproduction. Blood clotting seals wounds: platelets adhere to damaged tissue, a cascade of clotting factors activates thrombin, which converts soluble fibrinogen to insoluble fibrin, trapping erythrocytes in a mesh; the scab then protects while repair occurs - positive feedback in the platelet activation step, so it is a stock example of amplification.
Cell-mediated immunity: T lymphocytes (AQA 3.2.4; OCR 4.1.1; WJEC C3)
Cell-mediated immunity responds to cells displaying foreign antigens - body cells infected by viruses, cells altered by mutation (cancer cells), transplanted cells and APCs. Sequence: (1) a complementary T-helper cell binds to the antigen displayed on an APC (via its CD4 receptor and specific antigen receptor); (2) the APC activates the T-helper cell, which clonally expands by mitosis into a clone of active T-helper cells and memory T cells; (3) active T-helper cells stimulate specific B cells (humoral response) and phagocytes (enhanced phagocytosis) by releasing cytokines; (4) T-cytotoxic (killer) cells bind to complementary antigens on virus-infected or tumour cells and destroy them by releasing perforin, which makes pores in the target membrane so water flows in and the cell lyses. T-cytotoxic cells are the only cells that kill infected body cells directly - a key distinction from B cells (which produce antibodies against free pathogens). Memory T cells provide rapid cell-mediated secondary responses. HIV destroys T-helper cells, collapsing both arms of specific immunity (see below) - explaining why AIDS leaves patients vulnerable to opportunistic infections.
Humoral immunity: B lymphocytes and antibodies (AQA 3.2.4; OCR 4.1.1; CCEA AS2)
Humoral immunity responds to antigens free in body fluids (blood, lymph). Sequence: (1) specific B cells with complementary antibodies on their surface bind the antigen; (2) activated T-helper cells release cytokines that stimulate the B cells to clonally expand by mitosis (clonal selection and expansion); (3) most differentiate into plasma cells, which secrete large quantities of specific antibodies into the blood (up to 2000 per second); (4) some become memory B cells, long-lived, providing the secondary response. Antibody structure: a Y-shaped protein of two heavy and two light polypeptide chains joined by disulfide bridges; the variable regions at the tips of the Y have a tertiary structure complementary to one specific antigen (like a lock and key), forming an antigen-antibody complex; the constant region binds phagocyte receptors and complement. Antibody action: agglutination (clumping pathogens so phagocytes engulf many at once), opsonisation (marking pathogens for phagocytes), neutralisation of toxins, and preventing pathogens binding to host cells. Always state the complementarity of the variable region to the antigen - the mark scheme rewards the specificity link, not just 'antibodies kill pathogens'.
Clonal selection and expansion is the process the mark schemes dissect: each naive B cell carries antibodies of one specificity on its surface; when a complementary antigen binds, that B cell is selected; cytokines from T-helper cells stimulate it to divide by mitosis, producing a clone of genetically identical cells; the clone differentiates into plasma cells (antibody secretion) and memory B cells (secondary response). This is why the response is specific and why vaccination works - the vaccine antigen selects the complementary clones without disease. Antigen-antibody complexes are then cleared: agglutinated pathogens are engulfed by phagocytes, and the complexes can also activate complement proteins that lyse bacteria - quote agglutination, opsonisation and neutralisation of toxins as the three antibody actions.
Primary vs secondary response, vaccination and herd immunity (AQA 3.2.4; Edexcel A T6; OCR 4.1.1)
Interpret antibody concentration graphs: the primary response is slow - clonal selection and expansion take days to weeks; antibody concentration rises gradually, peaks, then falls as plasma cells die. The secondary response on re-exposure is faster, stronger and longer-lasting: memory B cells divide rapidly into plasma cells without needing T-helper activation of naive B cells, so high antibody concentrations are reached before symptoms develop (pathogen destroyed before it causes disease - the basis of immunity). Learn to read the graph axes and label both peaks; questions ask you to explain the difference in terms of memory cells, not just 'faster'.
Vaccination provides active artificial immunity: weakened, inactivated or fragment pathogens (or antigens/toxoids) are injected/taken orally, triggering the primary response so memory cells form without the person suffering disease; on natural exposure, the secondary response prevents symptoms. Herd immunity: when a high proportion of the population is vaccinated, pathogens cannot spread easily because most contacts are immune - protecting unvaccinated individuals (newborns, immunocompromised). The herd immunity threshold depends on how contagious the pathogen is (measles ~95%). Vaccination data interpretation (effectiveness, changing strains, uptake rates) appears on all boards. Active vs passive immunity: active - own immune system produces antibodies (infection or vaccination); slow onset but long-lasting with memory cells; passive - antibodies received from another organism (placental transfer, breast milk, antivenom, injected immunoglobulin); immediate but short-lived, no memory cells (antibodies are broken down). Learn the 2×2 grid: natural/artificial × active/passive, with one example each - a guaranteed definition-style question.
Vaccine types and interpretation: vaccines contain live attenuated pathogens (MMR - strong, long-lasting immunity), inactivated pathogens (flu - weaker, needs boosters), fragment/antigen vaccines (subunit - safest) or toxoids (inactivated toxins - tetanus); mRNA vaccines deliver genetic instructions for host cells to make the antigen. Herd immunity threshold depends on transmissibility (R₀): highly contagious pathogens (measles) need ~95% coverage, less contagious ones less - interpret vaccination-uptake and outbreak data from graphs, and evaluate why some vaccines fail (antigenic drift in flu and HIV, requiring updated vaccines annually) and why booster doses are needed (memory cell numbers decline over time).
Antibodies in medicine, HIV and antibiotics (AQA 3.2.4; OCR 4.1.1; Edexcel A T6)
Monoclonal antibodies are antibodies of one specificity produced by cloned B cells: a B cell (from a mouse immunised with the target antigen) is fused with a myeloma (tumour) cell to form a hybridoma, which divides endlessly and secretes identical antibodies; clones are screened and mass-cultured. Uses: ELISA tests (antibody-linked enzyme produces a colour change when the target antigen/antibody is present - pregnancy tests with HCG, HIV and pathogen testing, allergen testing), targeted therapy (monoclonals attached to toxic drugs/radioactive isotopes deliver treatment directly to tumour cells, reducing side effects), diagnosis (blood typing, cancer markers), and research. Ethics: animal use in production (mice immunised, tumour cells), informed consent in trials, and safety of attaching toxins. The ELISA sequence (capture antibody, antigen, detection antibody with enzyme, substrate) is examinable on AQA and OCR - know the wash steps and why controls are needed.
HIV is a retrovirus: RNA genome + reverse transcriptase inside a protein capsid, with a lipid envelope carrying attachment proteins (gp120). Replication: (1) gp120 binds complementary receptors (CD4) on T-helper cells; (2) the capsid enters the cell and uncoats; (3) reverse transcriptase converts viral RNA to DNA; (4) the DNA integrates into the host genome; (5) host enzymes transcribe viral RNA and translate viral proteins; (6) new viruses bud off, destroying or disabling the T-helper cell. Over years the T-helper count falls, collapsing both specific immune arms - AIDS - leaving opportunistic infections (TB, pneumonia) and cancers. HIV is transmitted in body fluids (blood, sexual contact, needles); initial infection may be asymptomatic for years, which is why testing (ELISA) matters. There is no cure (antiretroviral drugs slow replication); antibiotics do not work because viruses have no cell wall, ribosomes or bacterial metabolism to target. Antibiotics target bacterial-specific structures: cell wall synthesis (penicillin - prevents peptidoglycan cross-linking, so bacteria lyse osmotically), ribosomes (70S - tetracycline, protein synthesis blocked), DNA/RNA enzymes. Resistance arises by random mutation (e.g. penicillinase production) and spreads by natural selection and plasmid transfer: resistant bacteria survive antibiotic courses, reproduce and pass resistance genes vertically (binary fission) and horizontally (conjugation/plasmids). Overuse and incomplete courses increase the selection pressure - the standard evolution link (AQA 3.8, 3.7.3; OCR 4.1.1), and the basis of AQA RP6 (aseptic technique, antibiotic discs on bacterial lawns).
💡 Worked Example
Exam-style: AQA-style (3.2.4, 6 marks): Describe how phagocytosis of a pathogen leads to activation of the specific immune response.
Mark-scheme logic: Model answer logic (1 mark per point, 6 total): (1) Phagocytes are attracted to the pathogen by chemicals it releases (chemotaxis). (2) The phagocyte engulfs the pathogen, enclosing it in a phagosome formed from the cell-surface membrane. (3) Lysosomes fuse with the phagosome, releasing hydrolytic enzymes. (4) The enzymes digest the pathogen; soluble products are absorbed. (5) The phagocyte becomes an antigen-presenting cell, displaying the pathogen's antigens on its cell-surface membrane. (6) The displayed antigens stimulate complementary T-helper cells (cell-mediated immunity), which activate specific B cells to clonally expand and differentiate into antibody-secreting plasma cells (humoral immunity).
❓ Practice Questions & Mark Schemes
Describe the process of phagocytosis and explain how it leads to activation of the specific immune response. (6 marks)
Answer: Phagocytes are attracted to pathogens by released chemicals (chemotaxis) and engulf them, forming a phagosome from the cell-surface membrane. Lysosomes fuse with the phagosome, releasing hydrolytic enzymes (e.g. lysozyme) that digest the pathogen. Soluble products are absorbed and the phagocyte presents the pathogen's antigens on its cell-surface membrane (antigen-presenting cell). These antigens stimulate complementary T-helper cells (cell-mediated immunity). T-helper cells clonally expand and release cytokines, activating specific B cells. B cells clonally expand and differentiate into antibody-secreting plasma cells (humoral immunity).
Explain how the structure of an antibody is related to its function. (4 marks)
Answer: Y-shaped protein of two heavy and two light polypeptide chains joined by disulfide bridges. Variable regions have a tertiary structure complementary to one specific antigen, forming antigen-antibody complexes - confers specificity. Constant region binds phagocyte receptors, promoting phagocytosis (opsonisation). Two antigen-binding sites allow agglutination - clumping pathogens for more efficient phagocytosis.
Compare the primary and secondary immune responses. (5 marks)
Answer: Primary: slow onset - clonal selection and expansion of naive B cells take days to weeks; antibody concentration rises gradually, peaks then falls as plasma cells are short-lived. Secondary: much faster because memory B cells divide rapidly into plasma cells on re-exposure without naive activation. Stronger - higher peak antibody concentration. Longer-lasting - antibodies persist above the protection threshold. Symptoms are prevented because the pathogen is destroyed before it multiplies enough to cause disease.
Explain how vaccination leads to immunity and why it protects the unvaccinated. (5 marks)
Answer: Vaccines contain weakened, inactivated pathogens, antigens or toxoids. They trigger the primary immune response without causing disease. Clonal selection and expansion produce plasma cells (antibodies) and memory B/T cells. On natural exposure, memory cells enable a faster, stronger secondary response that destroys the pathogen before symptoms develop (active immunity). Herd immunity: with a high proportion vaccinated, pathogens cannot spread because most contacts are immune, protecting unvaccinated individuals such as newborns and the immunocompromised.
Explain why antibiotics are ineffective against viruses but effective against bacteria. (4 marks)
Answer: Antibiotics target structures specific to bacteria: cell wall synthesis (penicillin prevents peptidoglycan cross-linking so bacteria lyse osmotically), 70S ribosomes and bacterial enzymes. Viruses have no cell wall, no ribosomes and no metabolism of their own - they replicate using host cell machinery. So antibiotics have no target in viruses; antiviral drugs must instead target viral enzymes (e.g. reverse transcriptase) or host-cell factors.
Describe the structure of HIV and explain how it replicates in T-helper cells. (6 marks)
Answer: HIV is a retrovirus: RNA genome with reverse transcriptase inside a protein capsid, surrounded by a lipid envelope with attachment proteins (gp120). Attachment proteins bind complementary CD4 receptors on T-helper cells. The capsid enters and uncoats, releasing RNA and reverse transcriptase. Reverse transcriptase converts viral RNA into DNA, which integrates into the host genome. Host enzymes transcribe and translate viral proteins; new viruses assemble and bud off, destroying the T-helper cell. Loss of T-helper cells collapses both specific immune responses, causing AIDS.