Immune System – Dr Tracey Classens

Blood Components

The Four Units

🩸 Blood: The Body's Transport & Defence Network

Blood is a connective tissue — a liquid matrix called plasma that carries three types of cells and cell fragments. An adult human has approximately 5 litres of blood. Each component has a specific, non-negotiable role. Together they transport, defend, and repair.

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Component 1 — 55% of Blood Volume

Plasma — The Transport Fleet

Carries everything. Composed of 90% water. Never stops moving.

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🧪 Composition

~90% water — the solvent for everything
Plasma proteins: fibrinogen (clotting), antibodies (immunity), albumin (osmotic pressure)
Dissolved nutrients: glucose, amino acids, fatty acids, vitamins
Waste products: urea, CO₂ (as bicarbonate ions)
Hormones, ions (Na⁺, K⁺, Ca²⁺), gases

🚛 What It Transports

Digested food from intestines to liver and cells
Hormones from endocrine glands to target organs
Waste products from cells to kidneys and lungs
Heat — distributes body heat from active tissues
Clotting factors to sites of injury

🎯 Intel Brief

Serum = plasma with the clotting factors (fibrinogen) removed. This distinction appears in IEB questions about blood typing and laboratory tests. Blood serum is what remains after blood clots — clear yellowish fluid without fibrinogen.

55% of blood volume 90% water Contains fibrinogen, antibodies, albumin Serum = plasma minus clotting factors

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Component 2 — 45% of Blood Volume

Erythrocytes — The Oxygen Carriers

No nucleus. Biconcave disc. Lives 120 days. Carries 280 million haemoglobin molecules.

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🔬 Structure — Built for One Job

No nucleus — maximises space for haemoglobin
Biconcave disc shape — increases surface area for gas exchange; allows flexibility to squeeze through capillaries
No mitochondria — uses anaerobic respiration so it doesn't consume the O₂ it carries
Packed with haemoglobin (Hb) — iron-containing protein

⚙️ How Haemoglobin Works

In lungs (high O₂): Hb + 4O₂ → oxyhaemoglobin (bright red)
In tissues (low O₂): oxyhaemoglobin releases O₂ → deoxyhaemoglobin (dark red)
Also carries some CO₂ as carbaminohaemoglobin
Most CO₂ carried dissolved in plasma as HCO₃⁻ ions

🎯 Intel Brief

RBCs have no nucleus or organelles — they cannot divide or repair themselves. They live ~120 days, then are destroyed in the spleen. New ones are made in red bone marrow. The lack of a nucleus means RBCs cannot undergo mitosis — this is a classic exam question linking cell structure to function.

⚠️ Exam Trap

Carbon monoxide (CO) binds to haemoglobin 240× more strongly than oxygen — forming carboxyhaemoglobin. The Hb can no longer carry O₂, causing oxygen deprivation. This is why CO is lethal even in small amounts. IEB links this to pollution and gas poisoning questions.

Biconcave, no nucleus No mitochondria Carries haemoglobin Lives ~120 days Made in red bone marrow

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Component 3 — Less than 1% of Blood Volume

Leucocytes — The Defence Force

Have a nucleus. Can leave blood vessels. Outnumbered 700:1 by red cells — but run the entire immune system.

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🪖 Neutrophils — First Responders

Most numerous WBC (~60–70%)
Phagocytes — engulf and destroy bacteria and debris
First cells to arrive at infection sites
Multi-lobed nucleus — classic identifying feature
Short-lived (hours to days)

🧠 Lymphocytes — The Specialists

20–30% of WBCs
B lymphocytes — produce antibodies (humoral immunity)
T lymphocytes — destroy infected cells, coordinate immune response (cellular immunity)
Large round nucleus, little cytoplasm
Responsible for immunological memory

🐘 Monocytes → Macrophages

Largest WBC type
Leave blood → become macrophages in tissues
Engulf pathogens, dead cells, debris (phagocytosis)
Present antigens to lymphocytes — link innate and adaptive immunity

🔬 Key WBC Features

All have a nucleus (unlike RBCs)
Can perform diapedesis — squeeze through capillary walls into tissues
Produced in bone marrow (and thymus for T cells)
Number increases during infection (leukocytosis)

🎯 Intel Brief

The key WBC distinction for exams: Phagocytes (neutrophils, macrophages) are non-specific — they engulf anything foreign. Lymphocytes are specific — B cells produce antibodies against one specific antigen; T cells target specific infected cells. This specific vs non-specific distinction runs through the entire immune system.

All have nucleus Neutrophils = phagocytes B cells = antibodies T cells = cellular immunity Diapedesis into tissues

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Component 4 — Cell Fragments

Thrombocytes — The Repair Crew

Not full cells. No nucleus. One mission: seal the breach before the enemy gets in.

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🩹 The Clotting Cascade

Vessel damaged → platelets adhere to exposed collagen
Platelets release clotting factors + become sticky
Platelet plug forms at wound site
Clotting factors activate prothrombin → thrombin
Thrombin converts fibrinogen → fibrin threads
Fibrin net traps RBCs → clot (scab) forms

🔬 Structure & Facts

Fragments of large cells called megakaryocytes (in bone marrow)
No nucleus — cannot divide
Smallest formed elements in blood
Live ~7–10 days
Normal count: 150,000–400,000 per mm³ of blood

🎯 Intel Brief

The clotting sequence to know: Damage → platelet plug → prothrombin → thrombin → fibrinogen → fibrin → clot. Fibrinogen is a soluble plasma protein. Fibrin is the insoluble mesh that holds the clot together. Vitamin K is essential for producing clotting factors — its deficiency causes prolonged bleeding.

⚠️ Exam Trap

Haemophilia is a genetic disorder where clotting factor VIII (or IX) is absent or deficient. Blood cannot clot properly. It is X-linked recessive — mostly affects males. Distinguish from thrombocytopenia (too few platelets) and from normal clotting.

Cell fragments, no nucleus Fibrinogen → fibrin Prothrombin → thrombin Vitamin K needed for clotting

Lines of Defence

Three Perimeters

🛡️ The Body's Three Defence Perimeters

The immune system operates in three layers — each one more targeted than the last. The first two lines are non-specific (they don't care what the pathogen is — they attack everything). The third line is specific — it identifies the exact enemy and builds a custom weapon against it. This is the distinction that runs through every immune system exam question.

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First Line of Defence

Physical & Chemical Barriers — Keep Them Out

🏰 Physical Barriers

Skin — tough, multilayered barrier; keratin makes it waterproof and resistant to most pathogens
Mucous membranes — line respiratory, digestive, urinary tracts; trap pathogens in mucus
Cilia — hair-like projections in airways sweep mucus and trapped pathogens away from lungs
Earwax — sticky, antimicrobial; traps debris in ear canal

⚗️ Chemical Barriers

Stomach acid (HCl) — pH 1.5–2; destroys most ingested pathogens
Lysozyme — enzyme in tears, saliva, mucus; breaks down bacterial cell walls
Sebum — oily secretion of skin; slightly acidic; inhibits bacterial growth
Normal flora — beneficial bacteria on skin and in gut compete with pathogens

🎯 Intel Brief

The first line is NON-SPECIFIC — it doesn't distinguish between different pathogens, it simply prevents entry. When this line is breached (a cut, a burn, an inhaled pathogen getting past cilia), the second line is immediately activated.

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Second Line of Defence

Innate Immune Response — Non-Specific Counterattack

🔥 Inflammation Response

Damaged cells release histamine and other chemical signals
Blood vessels dilate → more blood to area → redness and heat
Increased capillary permeability → fluid leaks into tissue → swelling
Pain receptors stimulated → pain signal
4 cardinal signs: redness, heat, swelling, pain

🌡️ Fever Response

Pyrogens (from pathogens or WBCs) reset the hypothalamus thermostat
Body temperature rises — inhibits pathogen reproduction
Speeds up enzyme activity in immune cells
Promotes WBC production
Dangerous above 40°C — proteins begin to denature

🧹 Phagocytosis

Neutrophils and macrophages detect chemical signals from pathogens
Move toward pathogen (chemotaxis)
Engulf pathogen in a phagosome vesicle
Lysosomes fuse → enzymes destroy pathogen
Debris expelled or recycled

🛡️ Complement System

Proteins in plasma that are activated by pathogens
Puncture pathogen cell membranes
Flag pathogens for destruction (opsonisation)
Trigger inflammation
Work alongside antibodies in specific immunity

🎯 Intel Brief

The second line is still NON-SPECIFIC — phagocytes don't care what the pathogen is, they eat it. But this line also activates the third line by presenting antigens from destroyed pathogens to lymphocytes. Macrophages are the critical bridge between non-specific and specific immunity.

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Third Line of Defence

Adaptive Immune Response — Specific, Targeted, Remembered

🧬 B Lymphocytes — Humoral Immunity

Activated by specific antigen on pathogen surface
Proliferate → plasma cells (produce antibodies) + memory B cells
Antibodies bind to antigens → neutralise, agglutinate, flag for destruction
One B cell = one specific antibody type
Memory cells remain for rapid response to future infection

⚔️ T Lymphocytes — Cellular Immunity

Helper T cells (CD4⁺) — coordinate immune response; activate B cells and cytotoxic T cells; destroyed by HIV
Cytotoxic T cells (CD8⁺) — kill virus-infected cells and tumour cells directly
Memory T cells — persist for years; enable rapid secondary response
Mature in the thymus gland

⚠️ HIV & AIDS — The War Room's Greatest Threat

HIV (Human Immunodeficiency Virus) targets and destroys Helper T cells (CD4⁺ T lymphocytes). As T cell count falls, the entire specific immune response is progressively disabled. AIDS is diagnosed when CD4⁺ count falls below 200 cells/mm³ and the body can no longer fight opportunistic infections. This is why AIDS patients die from diseases that a healthy immune system would easily control.

Specific immunity B cells → antibodies T cells → cell-mediated Memory cells → long-term protection HIV destroys Helper T cells

Immune Response

Primary & Secondary

⚔️ How the Body Fights Back — And Remembers

The adaptive immune response has two versions: the primary response (first encounter with a pathogen — slower, takes days to build up) and the secondary response (subsequent encounters — faster and stronger because of memory cells). This difference is the biological basis of vaccination.

Day 0

Pathogen enters body — first infection

Antigen (foreign protein on pathogen surface) detected. First and second line defences activated immediately.

Days 1–3

Antigen presentation — macrophages brief the specialists

Macrophages engulf pathogens and display antigen fragments on their surface. Helper T cells recognise and bind to the antigen. The specific immune response is now activated.

Days 4–7

Clonal selection and expansion

The specific B cell and T cell recognising this antigen are activated and multiply rapidly (clonal expansion). B cells differentiate into plasma cells (antibody factories) and memory B cells.

Days 7–14

Antibody production peaks — pathogen defeated

Antibody levels rise, neutralising and flagging pathogens for destruction. Cytotoxic T cells kill infected cells. Symptoms typically peak then resolve as pathogen is eliminated.

Weeks later

Memory cells persist — immunological memory established

Most plasma cells and effector T cells die. Memory B and T cells survive for years — sometimes a lifetime. Antibody levels drop but memory remains.

Re-infection

Secondary response — faster, stronger, often symptom-free

Memory cells recognise the antigen immediately. Antibody production begins within hours, reaches higher levels, and lasts longer. Pathogen is neutralised before symptoms develop — immunity is achieved.

💉 Vaccination — Training the Army Without a Real Battle

A vaccine introduces a harmless form of the antigen (killed/weakened pathogen, or just the antigen protein) into the body. The immune system mounts a primary response and creates memory cells — without the person getting sick. If the real pathogen ever arrives, the secondary response eliminates it rapidly.

Active immunity: Body produces its own antibodies — from natural infection or vaccination. Long-lasting because memory cells form.

Passive immunity: Ready-made antibodies transferred into the body (e.g. mother's antibodies to foetus via placenta, or injected antiserum). Immediate but short-lived — no memory cells form.

Feature	Primary Response	Secondary Response
Trigger	First exposure to antigen	Re-exposure to same antigen
Speed	Slow — days to weeks	Rapid — hours to days
Antibody level	Low to moderate	High — much greater magnitude
Duration	Antibodies decline after infection	Antibodies persist longer
Symptoms	Usually present	Often absent or very mild
Memory cells	Formed during this response	Already present — rapidly activated

When the War Room Fails

Disorders & Diseases

🦠 HIV & AIDS

HIV (Human Immunodeficiency Virus) is a retrovirus that uses Helper T cells (CD4⁺) as its host. It inserts its RNA genome into the T cell's DNA, producing new viruses that destroy the host cell. Over years, CD4⁺ count drops from ~1000 cells/mm³ to below 200 — at which point AIDS (Acquired Immunodeficiency Syndrome) is diagnosed. ARV (antiretroviral) treatment suppresses viral replication but does not cure the infection.

Transmission: unprotected sexual contact, sharing needles, blood transfusion, mother to child (pregnancy, birth, breastfeeding). NOT through casual contact.

🤧 Allergies — Friendly Fire

An allergy is an overreaction of the immune system to a harmless substance (allergen — pollen, dust, peanuts). The immune system produces IgE antibodies against the allergen, causing mast cells to release histamine. Histamine causes inflammation, sneezing, itching, and in severe cases, anaphylaxis (potentially fatal whole-body reaction).

Treatment: Antihistamines block histamine receptors. Adrenaline is used for anaphylaxis — it reverses the dangerous drop in blood pressure and airways constriction.

🩸 Anaemia — Insufficient Firepower

Anaemia results from too few RBCs or insufficient haemoglobin — reducing the blood's oxygen-carrying capacity. Causes include iron deficiency (haemoglobin requires iron), vitamin B12 deficiency, blood loss, or destruction of RBCs (haemolytic anaemia). Symptoms: fatigue, pallor, shortness of breath.

Sickle cell anaemia: Genetic mutation changes one amino acid in haemoglobin — RBCs become sickle-shaped, blocking capillaries and being destroyed faster than they can be replaced. A classic IEB genetics-meets-physiology question.

🩺 Leukaemia — Mutiny

Leukaemia is cancer of the blood — uncontrolled production of abnormal, non-functional WBCs in bone marrow. These crowd out normal blood cell production, causing anaemia (fewer RBCs), increased bleeding (fewer platelets), and suppressed immune function (normal WBCs displaced). Treated with chemotherapy and bone marrow transplant.

💡 The 5 Things Examiners Want You to Know

1. Non-specific vs specific immunity — know which cells and processes belong to each line and why the distinction matters.

2. RBCs have no nucleus or mitochondria — structure is linked directly to function (maximise haemoglobin space, don't consume O₂ they carry).

3. The clotting sequence: damage → platelet plug → prothrombin → thrombin → fibrinogen → fibrin → clot.

4. B cells produce antibodies (humoral). T cells destroy infected cells (cellular). Memory cells provide immunological memory for both. Helper T cells coordinate both branches — and are destroyed by HIV.

5. Primary vs secondary response — secondary is faster and stronger because of memory cells. Vaccination exploits this mechanism.

🎯 War Room Debrief

Eight questions. No backup. Show what you know.

Question 1 of 8

Why do red blood cells have no nucleus or mitochondria?

Question 2 of 8

What is the correct sequence of events in blood clotting?

Question 3 of 8

A patient's immune system is mounting a response against a bacterial infection. Which cells are responsible for producing antibodies?

Question 4 of 8

The four cardinal signs of inflammation are redness, heat, swelling, and pain. What causes the SWELLING?

Question 5 of 8

Why does the secondary immune response produce a faster, stronger response than the primary response?

Question 6 of 8

HIV specifically destroys Helper T cells. Why does this eventually prevent the body from fighting ANY infection?

Question 7 of 8

What is the difference between active and passive immunity?

Question 8 of 8

Carbon monoxide poisoning is dangerous because CO binds to haemoglobin. What is the consequence of this binding?

The War Room:Blood & Immune System

Blood Components

🩸 Blood: The Body's Transport & Defence Network

🧪 Composition

🚛 What It Transports

🔬 Structure — Built for One Job

⚙️ How Haemoglobin Works

🪖 Neutrophils — First Responders

🧠 Lymphocytes — The Specialists

🐘 Monocytes → Macrophages

🔬 Key WBC Features

🩹 The Clotting Cascade

🔬 Structure & Facts

Lines of Defence

🛡️ The Body's Three Defence Perimeters

🏰 Physical Barriers

⚗️ Chemical Barriers

🔥 Inflammation Response

🌡️ Fever Response

🧹 Phagocytosis

🛡️ Complement System

🧬 B Lymphocytes — Humoral Immunity

⚔️ T Lymphocytes — Cellular Immunity

Immune Response

⚔️ How the Body Fights Back — And Remembers

💉 Vaccination — Training the Army Without a Real Battle

When the War Room Fails

🦠 HIV & AIDS

🤧 Allergies — Friendly Fire

🩸 Anaemia — Insufficient Firepower

🩺 Leukaemia — Mutiny

💡 The 5 Things Examiners Want You to Know

🎯 War Room Debrief

The War Room:
Blood & Immune System