Immune SystemOxford AQA IGCSE Biology: Revision notes

The body has non-specific defences that act as a first line of protection against all pathogens. These barriers prevent pathogens from entering the body or destroy them before they can cause infection.

Physical and chemical barriers:

• Skin acts as a physical barrier; it is impermeable to most pathogens and has a slightly acidic pH that inhibits bacterial growth
• Mucus is secreted by mucous membranes in the respiratory and digestive tracts; it traps pathogens and contains lysozyme (an antibacterial enzyme)
• Cilia are hair-like structures on cells lining the airways; they beat to move mucus and trapped pathogens away from the lungs
• Stomach acid (hydrochloric acid) denatures proteins in pathogen cell membranes and cell walls, destroying them
• Tears contain lysozyme and wash away pathogens from the eyes

These defences are called non-specific because they work against all types of pathogens in the same way, regardless of what antigen the pathogen carries.

When pathogens breach non-specific defences, the specific immune response is triggered. This involves two main types of white blood cells:

Phagocytes (neutrophils and macrophages):

• Recognise pathogens in the blood and tissues
• Phagocytosis is the process by which phagocytes engulf pathogens:
  1. Phagocyte recognises a pathogen
  2. Cell membrane surrounds and engulfs the pathogen
  3. Pathogen is enclosed in a vacuole
  4. Lysosomes fuse with the vacuole and release digestive enzymes
  5. The pathogen is destroyed
• This is a rapid response but non-specific; phagocytes can engulf many different types of pathogens

Lymphocytes (B cells and T cells):

• Are specific to individual pathogens because they have receptors for particular antigens
• B lymphocytes produce antibodies, which are proteins specific to one antigen
• T lymphocytes include helper T cells (stimulate B cell production) and killer T cells (destroy infected cells)
• The response takes longer to develop but is more effective because antibodies are precisely matched to the pathogen's antigens

Key difference: Phagocytes provide immediate defence; lymphocytes provide targeted, specific defence that improves over time.

Antibodies are globular proteins produced by B lymphocytes in response to specific antigens. Each antibody is specific to one antigen, like a lock fitting only one key.

Structure and specificity:

• Antibodies have a variable region with a shape complementary to a specific antigen
• This ensures each antibody binds only to its matching antigen
• The antigen-antibody binding is highly specific and precise

How antibodies destroy pathogens:

Why antibodies are effective:

• Highly specific—each one targets only its matching antigen
• Can work together to clump pathogens
• Label pathogens for destruction by phagocytes
• Act quickly once produced in large numbers

Memory cells are long-lived white blood cells that provide long-term, specific immunity after the first exposure to a pathogen.

How memory cells form:

1. When a pathogen invades, B and T lymphocytes divide and produce plasma cells (which secrete antibodies immediately)
2. Some lymphocytes do not become plasma cells; instead, they become memory cells
3. Memory cells remain dormant in lymphoid tissues for years or even a lifetime

How memory cells provide long-term immunity:

• If the same pathogen invades again, memory cells respond much faster than in the first infection
• Memory cells rapidly differentiate into plasma cells that produce large quantities of specific antibodies
• The secondary response is faster, stronger, and produces longer-lasting antibodies than the primary response
• This is why we don't suffer from the same infectious disease twice (usually)

Key features of memory cells:

• Pathogen-specific—each memory cell 'remembers' a particular antigen
• Long-lived—can persist for decades
• Provide immunological memory—the basis of vaccination and immunity after natural infection
• Responsible for why second infections cause milder symptoms or no symptoms

This is why it is much rarer to catch chickenpox twice in your life—your memory cells provide lasting immunity.

Vaccines work by stimulating the specific immune response without causing disease.

How vaccines work:

1. A vaccine contains antigens (from pathogens) or inactivated/weakened pathogens
2. Antigens in the vaccine are recognised by the immune system
3. B lymphocytes produce antibodies against the vaccine antigens
4. Memory cells form, providing long-term immunity
5. If the real pathogen invades later, memory cells mount a rapid secondary response
6. The pathogen is destroyed before it can cause serious illness

Types of vaccines:

• Live attenuated: weakened versions of the pathogen (e.g. MMR)
• Inactivated: dead pathogens or their components (e.g. flu vaccine)
• mRNA: genetic instructions for making the pathogen's antigens (e.g. COVID-19 vaccines)

Benefits of vaccination:

• Provides immunity without the dangers of natural infection
• Prevents serious disease and complications
• Can eradicate diseases (e.g. smallpox)
• Reduces healthcare costs
• Protects vulnerable people through herd immunity

Herd immunity (community immunity):

• When a large percentage of the population is vaccinated, unvaccinated individuals are protected
• Pathogens cannot spread easily because most people are immune
• Vulnerable people (babies, immunocompromised) are indirectly protected
• Typically requires 85–95% population immunity (varies by pathogen)

Risks and side effects of vaccination:

• Minor: local pain at injection site, mild fever, temporary soreness
• Rare: allergic reactions, serious adverse effects
• Very rare serious side effects must be weighed against the far greater risks of the disease itself
• Some people cannot be vaccinated due to allergies or medical conditions

Evaluating vaccination: When evaluating vaccination, consider: individual protection vs. community protection; severity of the disease prevented; frequency and severity of side effects; uptake rates needed for herd immunity.

Antibiotics are medicines that kill bacteria or inhibit their growth. They have saved millions of lives since their discovery.

Discovery of penicillin:

• Alexander Fleming, a Scottish bacteriologist, discovered penicillin in 1928
• He observed that a mould called Penicillium notatum had contaminated one of his bacterial culture plates
• Bacteria around the mould had been killed
• Fleming recognised the potential of this antimicrobial substance and named it penicillin
• Penicillin was later purified and mass-produced, revolutionising medicine

How antibiotics work: Different antibiotics target different bacterial structures or processes:

• Cell wall disruption: Penicillin and cephalosporins bind to bacterial cell wall proteins and prevent cell wall synthesis, causing the cell wall to break down and the bacterium to die
• Protein synthesis inhibition: Tetracyclines and aminoglycosides bind to bacterial ribosomes and prevent protein synthesis, killing the bacterium
• DNA replication inhibition: Fluoroquinolones prevent bacterial DNA replication

Why antibiotics cannot treat viral infections:

Key point: Viruses replicate using host cell structures and enzymes. An antibiotic that damages viral structures would damage human cells too, causing poisoning. Therefore, antibiotics are useless against viruses.

Antibiotic resistance is the ability of bacteria to survive in the presence of an antibiotic that would normally kill them. This is a major public health threat.

How antibiotic resistance develops (through natural selection):

1. A population of bacteria is exposed to an antibiotic (e.g. during treatment)
2. Most bacteria die because the antibiotic targets their cell wall or ribosomes
3. Some bacteria have spontaneous mutations that confer resistance (e.g. a gene for an enzyme that breaks down the antibiotic)
4. These mutant bacteria survive the antibiotic treatment
5. Non-resistant bacteria are killed, removing competition
6. Resistant bacteria reproduce rapidly, as they have access to nutrients and no competitors
7. The population is now dominated by antibiotic-resistant bacteria
8. If the same antibiotic is used again, it is ineffective because most bacteria are now resistant

Key points about resistance:

• Resistance occurs through natural selection, not because bacteria learn or adapt intentionally
• Mutations conferring resistance already exist in bacterial populations—antibiotics simply select for them
• Resistance develops faster with overuse and misuse of antibiotics (incomplete courses, unnecessary prescriptions)
• Different antibiotics select for different resistance mechanisms

Reducing antibiotic resistance:

• Complete full courses of antibiotics (do not stop early, even if you feel better)
• Use antibiotics only when prescribed (do not demand antibiotics for viral infections)
• Improve hygiene to reduce infection rates
• Develop new antibiotics to replace ineffective ones
• Use combination therapies
• Track resistance patterns in hospitals

Real-world example: Methicillin-resistant Staphylococcus aureus (MRSA) is resistant to many antibiotics and causes serious hospital-acquired infections.

All new medicines must undergo rigorous testing to ensure they are safe and effective before use in patients. This process takes years and involves multiple stages.

Stage 1: Preclinical testing (laboratory and animal testing)

• Drugs are tested in test tubes and cell cultures to identify promising candidates
• Potential drugs are then tested on laboratory animals (mice, rats, dogs) to assess:
  • Efficacy (does it work?)
  • Toxicity (is it poisonous?)
  • Safe dose ranges
  • Side effects
• Drugs that pass preclinical testing proceed to human trials
• This stage can take 3–5 years

Stage 2: Clinical trials (human testing) Clinical trials proceed through phases:

Phase 1:

• Small group of healthy volunteers (20–100 people)
• Assess safety and dosage
• Identify side effects
• Determine how the body processes the drug

Phase 2:

• Larger group of patients with the target disease (100–500 people)
• Assess efficacy—does the drug work?
• Continue safety monitoring
• Refine dosage

Phase 3:

• Large, diverse group of patients (1000–5000 people)
• Compare drug against existing treatments or placebo
• Often double-blind trials: neither patients nor researchers know who receives the drug vs. control
• Confirm efficacy and monitor side effects

Phase 4 (post-marketing surveillance):

• Drug is approved and released to the public
• Continuous monitoring for long-term effects and rare side effects

Placebo and double-blind trials:

Why multiple stages are necessary:

• Preclinical testing identifies candidates but animal models do not perfectly predict human responses
• Phase 1 ensures basic safety in humans before larger trials
• Phase 2 and 3 confirm efficacy and identify common and rare side effects
• Large phase 3 trials detect side effects that would be missed in smaller studies
• Placebos and double-blind methods eliminate bias and the placebo effect