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You now know what pathogens are and how they spread. This lesson looks at how the body fights back, and at the two great medical tools that help it: vaccines and antibiotics. First, the body's own defences work in two lines: non-specific barriers try to keep pathogens out, and if they get in the white blood cells of the immune system attack them and leave behind memory cells that give immunity. Second, vaccination uses those memory cells to make us immune before we meet a dangerous pathogen, and antibiotics kill bacteria once they are inside us — though crucially they do not work on viruses, and antibiotic resistance is now a serious global problem. This is the heart of the health strand of Topic B6.
By the end of this lesson you should be able to describe the body's non-specific defences, explain the roles of white blood cells (phagocytosis, antibodies and antitoxins), explain how memory cells give immunity, explain how a vaccine works and what herd immunity is, and distinguish antibiotics from antivirals while explaining antibiotic resistance.
This lesson develops AO1 (understanding the immune response, vaccination and antibiotic resistance) and AO3 (interpreting antibody-response and herd-immunity data and evaluating the antibiotic-resistance problem).
Before the immune system is ever needed, the body tries to stop pathogens entering at all. These non-specific defences work against all pathogens, not just one, and include both physical and chemical barriers.
| Defence | Type | How it protects |
|---|---|---|
| Skin | Physical | A tough barrier; if cut, it scabs over to reseal. It also supports harmless bacteria that crowd out pathogens |
| Mucus and cilia in the airways | Physical | Sticky mucus traps pathogens and dust; tiny hairs called cilia sweep the mucus up and out of the lungs to be swallowed or removed |
| Stomach acid | Chemical | The stomach produces strong hydrochloric acid that kills most pathogens swallowed in food, drink or mucus |
| Tears | Chemical | Contain enzymes that kill bacteria on the surface of the eye, and also wash pathogens away |
| Nose | Physical | Hairs and mucus trap pathogens in inhaled air |
Exam Tip: These are non-specific defences — they work against any pathogen and are not "learned". Don't confuse them with the specific immune response (antibodies), which is targeted at a particular pathogen. A common question asks you to name two ways the body stops pathogens entering; mucus-and-cilia and stomach acid are reliable answers.
If a pathogen breaks through the barriers, the immune system responds. The key players are the white blood cells, which patrol the blood and tissues, and they defend the body in three ways.
Some white blood cells, called phagocytes, destroy pathogens by engulfing them. The phagocyte changes shape to surround the pathogen, takes it inside the cell, and then digests it using enzymes. Because phagocytes engulf any pathogen, this is a non-specific response.
Other white blood cells, called lymphocytes, make antibodies. Every pathogen carries unique marker molecules on its surface called antigens. A lymphocyte makes an antibody with a shape that is complementary to a specific antigen — the two fit together like a lock and key. The antibody locks onto the antigen, marking the pathogen for destruction and causing pathogens to clump together so they are easier to engulf.
Because each antibody fits only one type of antigen, this is a specific response: a particular antibody works against a particular pathogen and no other. This is also why being immune to one disease — chickenpox, say — gives you no protection against a different one such as measles: the antibodies you made have the wrong shape for the new pathogen's antigens, so the slow first response has to happen all over again.
Some white blood cells produce antitoxins. These are chemicals that neutralise the toxins released by bacteria, stopping the toxins damaging the body's cells. Antitoxins deal with the poisons a pathogen makes, rather than the pathogen itself.
A useful way to keep antibodies and antitoxins apart is to think about what each targets. Recall that some bacteria make us ill mainly through the toxins they release. Antibodies target the pathogen (by locking onto its antigens), while antitoxins target the toxins the pathogen produces. Both are made by white blood cells, but they tackle different parts of the problem — one the invader, the other its poisons.
| Term | What it is | Made by | What it does |
|---|---|---|---|
| Antigen | A marker molecule on the surface of a pathogen | The pathogen | Acts as the "identity tag" the immune system recognises as foreign |
| Antibody | A protein with a shape complementary to one antigen | The body's white blood cells (lymphocytes) | Locks onto the matching antigen, labelling and clumping pathogens for destruction |
| Antitoxin | A protein that binds to and neutralises a toxin | The body's white blood cells | Stops bacterial toxins damaging the body's cells |
Exam Tip: Keep the three white-blood-cell jobs distinct: phagocytosis engulfs and digests pathogens; antibodies lock onto antigens to label and clump pathogens; antitoxins neutralise bacterial toxins. Mixing up antibodies and antitoxins is one of the commonest slips in this topic.
When you meet a new pathogen, it takes a few days for the right lymphocyte to multiply and make enough of the correct antibody — which is why you feel ill at first. But once the infection is beaten, some of those lymphocytes remain as memory cells.
If the same pathogen ever enters the body again, the memory cells recognise its antigen at once and produce the correct antibody much faster and in greater quantity. The pathogen is destroyed before it can make you ill — you are now immune to that disease. This is exactly the principle that vaccines exploit.
Exam questions often give you a graph of antibody concentration against time like the one above and ask you to interpret it. Work through it the same way every time. After the first exposure there is a delay of several days before antibodies appear (the flat stretch near the start) — the time the lymphocytes need to find the matching antigen and divide. The curve then rises to a low peak and falls again as the infection is cleared. After the second exposure to the same antigen, three things change at once: antibodies appear sooner, they rise to a much higher peak, and the level stays raised for longer. If asked to compare the two responses, quote all three differences — faster, higher and longer-lasting — and then explain them by naming memory cells: a large population of matching memory cells is already present, so they recognise the antigen immediately and make antibodies in bulk, destroying the pathogen before it can cause symptoms.
Exam Tip: A question may ask why someone is ill for a few days with a new infection but not when they meet the same pathogen again. Link it to memory cells: the first time, lymphocytes must multiply before enough antibodies are made (so you are ill); the second time, memory cells make antibodies immediately, so the pathogen is destroyed before symptoms appear.
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