Unit 11 Immune system, vaccination and antibiotics
Key unit competence: Validate the immune system, vaccination and antibiotics for maintenance of a healthy body.
Key ideas
- Phagocytes are white blood cells made in the bone marrow from stem cells. Neutrophils (lobed nucleus, short-lived) circulate and arrive first at infections; monocytes leave the blood and become macrophages in tissues, which also present antigens. Phagocytosis: the phagocyte is attracted by chemicals (chemotaxis), binds the pathogen, engulfs it into a phagosome, lysosomes fuse and hydrolytic enzymes digest it.
- The immune system protects the body against pathogens (bacteria, viruses, fungi, protoctists). Innate (non-specific) immunity is present from birth and acts the same way against all pathogens. Acquired (specific) immunity develops after exposure to a specific antigen, involves lymphocytes, and produces memory.
- First line of defence (barriers): skin (keratin, sebum), mucous membranes and cilia, tears and saliva with lysozyme, stomach acid, normal skin and gut flora. Second line: phagocytosis, the inflammatory response (damaged cells and mast cells release histamine, causing vasodilation, leaky capillaries, redness, heat, swelling and pain, bringing phagocytes), fever, and antimicrobial proteins such as interferons (stop viruses spreading) and complement. Third line: specific lymphocyte responses.
- An antigen is a molecule (usually protein or glycoprotein) that triggers an immune response. Antibodies are Y-shaped immunoglobulins with two heavy and two light chains, a variable region forming two antigen-binding sites and a constant region. They act by agglutination, neutralising toxins, marking pathogens for phagocytes (opsonisation) and activating complement (lysis).
- B lymphocytes mature in bone marrow; T lymphocytes mature in the thymus. Humoral immunity: a B cell with the matching receptor is activated (with help from T helper cells), divides by mitosis (clonal selection and expansion) to form plasma cells, which secrete antibodies, and memory B cells. Cell-mediated immunity: T cells recognise antigens presented on cells; T helper cells release cytokines that activate B cells and phagocytes; T killer (cytotoxic) cells destroy infected or cancer cells (perforin); memory T cells form.
- The primary response is slow with few antibodies; the secondary response (on re-infection) is faster, stronger and longer-lasting because memory cells are ready. Types of immunity: natural active (after infection), artificial active (vaccination), natural passive (antibodies across the placenta or in colostrum/breast milk), artificial passive (injection of antibodies, e.g. anti-tetanus serum, antivenom). Active immunity is long-lasting with memory; passive is immediate but short-lived.
- Allergies are harmful immune responses to harmless antigens (allergens) such as pollen, dust mites, some foods, insect stings and drugs. On first exposure IgE antibodies attach to mast cells; on re-exposure the allergen binds, mast cells release histamine: sneezing, itching, rash, asthma, swelling. Severe whole-body reaction: anaphylaxis, treated with adrenaline. Prevention and management: avoid allergens, antihistamines, inhalers, desensitisation.
- Vaccination gives artificial active immunity by introducing antigens in a safe form. Types: live attenuated (measles, oral polio, BCG), inactivated/killed (injected polio), toxoid (tetanus, diphtheria), subunit (hepatitis B, HPV), mRNA (some COVID-19 vaccines). History: Edward Jenner (1796) used cowpox to protect against smallpox; smallpox was eradicated in 1980. Herd immunity: when most people are vaccinated, the pathogen cannot spread, protecting the unvaccinated. Limitations: antigenic variation (influenza, HIV), poor storage (cold chain), weak response in malnourished people, pathogens hiding inside cells, vaccine hesitancy.
- Antibiotics are chemicals made by microorganisms (or synthetic) that kill or inhibit bacteria but not human cells. Alexander Fleming discovered penicillin from the mould Penicillium (1928). Actions: bactericidal (kill, e.g. penicillin blocks cell wall synthesis, so bacteria burst by osmosis) or bacteriostatic (stop growth, e.g. tetracycline blocks ribosomes). Antibiotics do not work on viruses. Overuse and incomplete courses lead to antibiotic resistance (mutation + selection, e.g. MRSA). Prevent it by completing courses, avoiding unnecessary prescriptions and limiting use in livestock.
Common misconceptions
- "Antibiotics cure colds and flu." No: these are caused by viruses, which antibiotics do not affect.
- "Vaccines contain antibodies." No: vaccines contain antigens; the body makes its own antibodies (active immunity).
- "Passive immunity gives lasting protection." No: no memory cells form, so it lasts only weeks.
- "Bacteria become resistant because the person gets used to the drug." No: bacteria become resistant by mutation and natural selection.
Worked examples
Example 1. Explain why a second infection with the same measles virus usually causes no illness.
Solution
After the first infection, memory B and T cells remain. On re-infection they recognise the antigen and divide quickly, so plasma cells release large amounts of antibody much faster (secondary response). The virus is destroyed before symptoms develop.
Example 2. Explain why a patient should complete a course of antibiotics.
Solution
Stopping early leaves the most resistant bacteria alive. They multiply, and the population becomes resistant (natural selection). Completing the course kills nearly all bacteria, reducing the chance of resistant strains.
Practice questions
Describe the process of phagocytosis.
Show answer
Phagocyte attracted to pathogen by chemicals; binds to it; engulfs it by endocytosis into a phagosome; lysosomes fuse; hydrolytic enzymes digest the pathogen; products absorbed or released.
Common mistake: Saying phagocytes produce antibodies.
Describe the first line of defence of the body.
Show answer
Skin barrier with keratin; sebum; mucus and cilia in airways; lysozyme in tears and saliva; stomach acid; normal flora; blood clotting seals wounds.
Common mistake: Including antibodies in the first line.
Describe the inflammatory response.
Show answer
Damaged cells and mast cells release histamine; arterioles dilate; capillaries become leaky; plasma and phagocytes move to tissue; redness, heat, swelling, pain; pathogens destroyed.
Common mistake: Saying inflammation is caused by antibiotics.
Describe the humoral immune response.
Show answer
Antigen presented; T helper cells activate B cell with complementary receptor; clonal selection; B cells divide by mitosis; plasma cells secrete antibodies; memory cells form.
Common mistake: Saying T cells make antibodies.
Compare active and passive immunity.
Show answer
Active: body makes own antibodies, memory cells, long-lasting, slow to develop. Passive: antibodies given, no memory, short-lived, immediate.
Common mistake: Saying passive immunity lasts for life.
Explain how vaccination protects against disease.
Show answer
Vaccine contains antigens of a weakened, killed or part pathogen; primary response; memory cells form; on real infection a fast secondary response destroys pathogen before illness.
Common mistake: Saying vaccines kill pathogens directly.
Explain how an allergic reaction occurs.
Show answer
First exposure: IgE made and attaches to mast cells (sensitisation). Re-exposure: allergen binds IgE on mast cells; histamine released; vasodilation, swelling, itching, sneezing, bronchoconstriction.
Common mistake: Saying allergy happens on first contact.
Explain how antibiotic resistance develops and how it can be reduced.
Show answer
Random mutation gives a resistant bacterium; antibiotic kills non-resistant ones; resistant ones survive and reproduce; resistance spreads (also by plasmids). Reduce by completing courses, prescribing only when needed, limiting farm use, hygiene.
Common mistake: Saying people become resistant.
Matching and drag-and-drop
Matching
Match each item in column A with the correct answer in column B. Write the letter next to each number.
Column A Column B 1. Penicillin was discovered by: a. Alexander Fleming 2. A severe whole-body allergic reaction is: b. anaphylaxis 3. Antibodies are secreted by: c. toxoid vaccine 4. A tetanus vaccine is an example of a: d. plasma cells Show answer
1 → a (Alexander Fleming) · 2 → b (anaphylaxis) · 3 → d (plasma cells) · 4 → c (toxoid vaccine)
- From Penicillium mould.
- Treated with adrenaline.
- Derived from B cells.
- Inactivated toxin.
Drag and drop
Choose the correct word or phrase from the box for each gap. One word in the box is not needed.
artificial passive · Edward Jenner · artificial active · bone marrow- Phagocytes are made in the .
- The first vaccine was developed by .
- Immunity after a vaccine is .
Show answer
1: bone marrow · 2: Edward Jenner · 3: artificial active
- From stem cells.
- Using cowpox.
- The body makes antibodies.
Matching
Match each item in column A with the correct answer in column B. Write the letter next to each number.
Column A Column B 1. T lymphocytes mature in the: a. antigen 2. Clumping of bacteria by antibodies is: b. agglutination 3. Penicillin kills bacteria by blocking: c. cell wall synthesis 4. A molecule that triggers an immune response is an: d. thymus Show answer
1 → d (thymus) · 2 → b (agglutination) · 3 → c (cell wall synthesis) · 4 → a (antigen)
- T for thymus.
- It helps phagocytes.
- Bacteria burst by osmosis.
- Usually a protein.
Drag and drop
Choose the correct word or phrase from the box for each gap. One word in the box is not needed.
IgE · lysozyme · natural passive immunity · artificial passive immunity- An enzyme in tears that kills bacteria is .
- Anti-tetanus serum gives .
- The antibody involved in allergies is .
Show answer
1: lysozyme · 2: artificial passive immunity · 3: IgE
- It breaks bacterial walls.
- Ready-made antibodies.
- It binds mast cells.