Immunity
— Biology · AS Level (7402)
★ Exam Tip: Immunity is a short chapter but every part links to
the next: WBC types → antigen → phagocytosis → antigen presentation → humoral / cell-mediated
response → memory → vaccines → monoclonal antibodies. Learn it as one story, not separate topics.
1. Key Terms
| Term | Meaning |
|---|---|
| Pathogen | disease-causing organism (virus, bacteria, fungi) |
| Pathogenicity | disease-causing ability — an organism that has it is called a pathogen |
| Immune system | the body's internal defence system |
| Immunity | protection against diseases (e.g. you are "immune" to chicken pox after having it, or after vaccination) |
Remember: Organism = pathogen. Ability = pathogenicity. They are used
all the time in this chapter!
• Not all microbes are harmful — bacteria on the skin and in the gut live mutualistically with us. Only those which can make toxins / chemicals / harmful reactions are pathogens.
• The main cells of the immune system = WBCs (white blood cells) = leukocytes. Unlike RBCs (one type), WBCs have different types with different roles.
2. Classification of Leukocytes
① By FUNCTION (role in defence)
- Monocyte vs macrophage: a monocyte is the immature cell. When it matures and embeds in deep tissues / organs it becomes a macrophage (mature form).
- Phagocytes (neutrophils + monocytes/macrophages) → perform phagocytosis only. They do NOT make antibodies.
- Plasma cells → produce antibodies. B memory cells, TH / TK memory cells → remember the antigen so a second attack is stopped quickly.
- T-helper and T-killer cells — roles come later (both are lymphocytes).
Sir's analogy: antibodies = a guard at your house who chases off a
thief. Memory cells = the guard recognises the same thief instantly the next time.
Note: Eosinophils (fight infections — their count rises in a
blood test during infection) and basophils are not in the syllabus, so we don't study them. Focus:
phagocytes + lymphocytes.
② By APPEARANCE (under the microscope)
(1) Granulocytes — cytoplasm contains granules.
e.g. neutrophils,
basophils, eosinophils.
(2) Agranulocytes — cytoplasm is devoid of any visible granules.
e.g. monocytes,
lymphocytes.
Trick: prefix "a-" = absence of (a-granulo = no granules;
a-sexual; a-political).
| Cell type | Granules? | Nucleus |
|---|---|---|
| neutrophil, basophil, eosinophil | present | lobed (neutrophil: 3 lobes) |
| monocyte | absent | not round — lobed / bean-shaped (sir counted it with the lobed group) |
| lymphocytes (B, T, killer) | absent | large spherical nucleus |
3. Antigens & the Immune Response
Antigen: a macromolecule (usually a protein, not always) that can trigger an immune response. Antigens are cell recognition markers — glycoproteins on the cell surface membrane with a unique shape, like your ID card that tells the body "who this cell is".
Sir's blood-group example:
My blood is B+ → my RBCs carry antigen B. My WBCs
know antigen B = "my own people, no danger". If an A-group person donated blood to me, antigen A is foreign
→ my WBCs attack it, the donor RBCs clot, vessels get blocked → can cause death.
Self antigenNOT foreign to your body → will NOT trigger
an immune response ("apna banda — why harm it?")
Non-self (foreign) antigenforeign to your body → WILL
trigger an immune response immediately
Immune response: a complex series of reactions carried out by phagocytes and lymphocytes in response to a foreign (non-self) antigen.
Common mistake: only plasma cells (a type of B cell) make
antibodies. Phagocytes never make antibodies — they only engulf / digest.
4. The Defence System — 3 Lines of Defence
Think of border security: the 1st line of soldiers faces the enemy, the 2nd stands behind them, and the 3rd is the most advanced. (Or: a student reaching the principal goes through the CR first — a fixed channel.) The body protects itself at every level.
① External defence — no WBCs, non-specific, fixed & constant
| Type | Examples | How it protects |
|---|---|---|
| (1) Physical barriers | skin · nasal hair · cilia | skin separates outside from inside; nasal hair traps dust (sneezing); cilia brush particles out |
| (2) Chemical barriers | mucus · HCl | mucus = mucin (glycoprotein) + serous fluid, sticky → traps bacteria/dust, cilia sweep it out; HCl in gastric juice → acidity kills bacteria |
| (3) Cellular barriers | platelets (clotting mechanism) | at a cut, platelets trigger fibrinogen → fibrin mesh/web that seals the wound so pathogens can't enter |
Note: The same skin / mucus / HCl / clotting protects against
every foreign particle in exactly the same way — that is what "non-specific, fixed, constant" means. These
barriers are not part of the immune system itself; the immune system switches on only when a pathogen
enters the internal environment (blood).
② vs ③ Innate and Adaptive immune response
| Innate immune response | Adaptive immune response | |
|---|---|---|
| Cells involved | phagocytes (neutrophils, macrophages) | lymphocytes (B cells, T cells) |
| Specificity | non-specific — attacks any foreign particle | specific — only the antigen with a complementary receptor |
| Immunological memory | none | yes (memory cells) |
Why "no memory" for phagocytes? They just notice "a foreign particle
— eat it!" without caring what it is, so nothing specific is remembered. Lymphocytes get a specific receptor
shape at maturation → specific + memory.
5. Innate Immune Response — Phagocytosis
Done by neutrophils and macrophages (macrophages are the more important ones). Like a shark smelling prey from far away, or a sniffer dog following a scent — phagocytes follow chemical signals.
- Chemotaxis — chemo = chemical, taxis = movement: movement towards a chemical stimulus (chemicals released when a pathogen enters; histamine too) → phagocyte runs to the pathogen.
- Recognition + attachment — phagocyte recognises it as non-self (not my self-antigen) and sticks to it.
- Endocytosis / phagocytosis — membrane wraps around and engulfs the pathogen → a vesicle forms = phagocytic vesicle = phagosome (vesicle with the pathogen inside).
- Lysosome attaches to the phagosome → they fuse = phagolysosome.
- Lysosome secretes hydrolytic (digestive) enzymes into the vesicle → pathogen is digested.
- Remaining residual waste is removed by exocytosis.
Exam Tip: Know the difference: phagosome = just the vesicle
holding the pathogen. Phagolysosome = once a lysosome has fused with it and is releasing enzymes.
Keep the order: chemotaxis → recognition + attachment → endocytosis → phagosome → phagolysosome →
digestion → exocytosis.
If phagocytosis is NOT enough → Antigen Presentation
Sometimes at stage 5 the phagocyte realises the pathogen is too powerful (e.g. only 20–30% digested). It then shows the left-over pathogen as an antigen on its own cell surface — a call for help to the lymphocytes (3rd line of defence). This is antigen presentation, and the cell doing it is an antigen-presenting cell (APC).
- Only macrophages can do antigen presentation — neutrophils cannot.
- Antigen is fused into the cell surface membrane → connects innate to adaptive immunity.
- Only the lymphocyte with a complementary receptor can answer → the system becomes specific here.
Analogy: hospital emergency = phagocytes (treat
everyone). When it is a specialist case (neuro, nephro…), they refer to the specific doctor = the
matching T-helper cell.
6. Origin & Maturation of Lymphocytes
All blood cells (RBCs, WBCs, platelets) are made from stem cells in the bone marrow (that's why a bone marrow transplant can cure blood cancer / sickle-cell anaemia — healthy marrow replaces faulty marrow).
Memory: T cells mature in the Thymus.
| Production | Maturation | |
|---|---|---|
| T lymphocytes | bone marrow | thymus (gland in the upper chest near the thyroid) |
| B lymphocytes (and all other WBCs) | bone marrow | bone marrow |
• T cells leave marrow immature → travel to the thymus → mature → released into the bloodstream.
What does maturation do?
Glycoproteins on the cell surface = cell recognition markers = receptors. Each has a certain shape, so only a complementary-shaped molecule can bind. Immature cells have no receptors; during maturation each T cell gets a glycoprotein receptor placed on its surface (different shape on different cells).
B cell receptors = ANTIBODIES
- The glycoprotein receptor on the surface of a B cell is given a special name: antibody (the word is used for no other cell).
- An unspecialised B cell has antibodies on its surface but cannot release them into blood. It then specialises into plasma cell (can produce & release antibodies into blood) and B memory cell (keeps memory).
Trick: AntiBody → "AB" → there is a B in antibody →
antibodies belong to B cells.
Common mistake: "Every B cell has antibodies on its surface" ✓ — but
"every B cell can release antibodies into blood" ✗. Only plasma cells can.
7. Structure of an Antibody
| Feature | Detail |
|---|---|
| Type of molecule | glycoprotein, globular (soluble). Also called immunoglobulins. |
| Polypeptide chains | 4 — 2 light (globin) chains + 2 heavy (globin) chains (light/heavy = smaller/larger Mr) |
| Protein structure | quaternary (more than one polypeptide) |
| Bonds | disulfide bonds link the chains — each antibody has 16 (sir's number) |
Variable region (antigen-binding site)top of the Y — shape
varies for every antibody; complementary to one antigen
Constant regionrest of the Y — common to all antibodies;
no antigen binds here
Why must the variable region differ?
Millions of B cells → each has its own antibody
shape → each antibody fits its own antigen. If all shapes were the same, the body couldn't tell which antibody
should attack the virus and which the bacteria. Like enzymes: specific to their substrate.
The constant region & OPSONISATION
The "lollipop" receptors on the constant region help phagocytes. When a pathogen enters, chemicals (mostly histamine) signal it; antibodies attach to the pathogen by their variable region and coat its surface. Because antibodies are glycoproteins → sugars → sticky, the coat makes it easy and strong for a phagocyte to attach and engulf. This is opsonisation.
Sir's kitchen analogy: to stick breadcrumbs on dough you first dip
it in egg / water; to stick two layers you brush a liquid between them. The antibody coat is that sticky
layer.
Common mistake: "If antibodies already attack the antigen, why do we
need phagocytes?" — Phagocytes are non-specific and need help attaching. The variable region does
the specific binding; the constant region + sticky sugar just makes phagocyte attachment easier. Don't
confuse the two jobs.
8. Functions of Antibodies
- Opsonisation — coat the pathogen surface to promote effective phagocytosis (constant region).
- Bind to viruses → prevent their entry into the host cell.
- Bind to toxins and neutralise them (e.g. toxins released by bacteria) → such antibodies are antitoxins.
- Bind to the flagellum of bacteria → restrict bacterial motility.
- Punch holes in the cell wall of bacteria (like a punching machine) → water enters → bacterium bursts = cell lysis (lysis = bursting / breaking apart).
- Clump antigens together → agglutination (antigens stuck in a big clump).
9. Adaptive Immune Response
Carried out by lymphocytes (B cells + T cells). Both have glycoprotein receptors from maturation → specific. B-cell receptors = antibodies. It has two types:
① Humoral (antibody-mediated)done by B cells (via
antibodies) — against pathogens in the blood
② Cell-mediateddone by T-killer cells — against
cancerous (tumour) cells and/or virus-infected cells
"Mediated" = the connecting link that carries out the response. Antibody-mediated → antibody does it; cell-mediated → a particular cell does it.
Link from phagocytosis: APC shows antigen → T-helper cell
with a complementary receptor binds (not T-killer, plasma or memory cells!). T-helper then decides which response:
humoral (pathogen) or cell-mediated (virus-infected / tumour cell).
A) Humoral (antibody-mediated) response — step by step
Sir's emergency analogy: the T-helper asks the APC "what help do you
need?" → "I know someone who can do this — the B cell." Cytokines = the message sent to that B cell.
Clone = a group of identical cells (like identical twins). We stimulate only the clone whose antibody receptor is complementary to the antigen, then make more copies — more are needed now (plasma cells) and some stored for later.
① CLONAL SELECTIONT-helper cells secrete cytokines to
stimulate the clone of B cells with a complementary antibody receptor
② CLONAL EXPANSIONrapid division by mitosis → numerous
identical cells
③ DIFFERENTIATION→ plasma cells: production + secretion of
numerous identical antibodies (into blood) · → B memory cells: reside in the lymph nodes,
retain immunological memory (insurance for the second attack)
Vaccine link (COVID):
a weakened/dead pathogen is injected; your immune system treats it as
a real threat → plasma cells make antibodies and memory cells remain. You needn't actually catch the disease.
B) Cell-mediated response — T-killer cells
Used against virus-infected cells and tumour (cancer) cells. (Tumours: mutation in cell-division genes → uncontrolled mitosis → irregular mass; the body fights them via the immune response, or by apoptosis — see mitosis notes.)
- APC displays a viral or tumour antigen; a complementary T-helper cell binds → releases cytokines (chemical signals).
- Clonal selection of the clone of T-killer cells with complementary receptors.
- Clonal expansion via mitosis.
- Differentiate into activated TK cells and TK memory cells (memory for 2nd/3rd exposure — skips the whole long cycle).
- Activated TK cells bind to the antigens and destroy the cell bearing them: their vacuoles release hydrogen peroxide (H₂O₂) and interferons which punch holes in the cell membrane of the affected cell → cell lysis / death.
Don't mix up: T-helper cytokines → B cells (humoral) or
T-killer cells (cell-mediated). T-killer cells don't make antibodies — they kill the cell directly.
★ Exam Tip — full story to learn: pathogen → barriers (no WBCs) →
phagocytosis (innate) → if it fails: antigen presentation → T-helper → cytokines → humoral (B
cells: plasma + memory) or cell-mediated (T-killer + memory). Memory cells give the faster 2nd
response.
10. Types of Immunity
| Type | What happens | Example |
|---|---|---|
| Natural active | pathogen enters naturally from the environment → immune system makes its own antibodies; no human intervention | catching chicken pox |
| Artificial active | vaccination — dead / weakened (attenuated) pathogen injected; body doesn't know it's harmless → makes antibodies itself | polio, measles, COVID vaccines |
| Natural passive | baby gets mother's antibodies via the placenta (blood systems linked) and via breast-feeding (milk has strong antibodies) | newborn protection |
| Artificial passive | ready-made antibodies injected from an external source (e.g. extracted from an animal's serum, then humanised so the body won't reject it) | antibody injection |
Sir's memory trick: Active = you work for your antibodies.
Passive = antibodies are "served on a plate" — so it is short-lived.
11. Vaccination (Artificial Active Immunity)
Definition: a medical service in which an injection containing antigen is given to achieve artificial active immunity (→ antibody production).
Types of vaccine
- Killed whole-cell pathogens (dead pathogen)
- Live vaccines — weakened (attenuated) pathogen; disease-causing ability removed
- Microbial subunit vaccine (and toxoid vaccine)
- Genetically engineered vaccines
What makes a GOOD vaccine?
- Low toxicity
- Stimulates both humoral and cell-mediated responses
- Thermostable (no fridge chain needed)
- Easy to produce and cheap
- Effective in all age groups and ethnicities
- No need for boosters
Booster doses
First dose → antibodies rise (e.g. 0 → 10 units) but not enough. A booster (2nd dose of the same vaccine) raises antibody concentration to the required level. It works well because plasma cells, antibodies and memory cells already exist — memory cells recognise the antigen at once, so only a "boost" is needed (like a new employee inheriting half-finished work). Analogy: your energy low in the afternoon, then boosted by good news.
Problems associated with vaccines
| Problem | Why |
|---|---|
| 1. Poor response to vaccine | Malnourishment — antibodies are glycoproteins (protein-based); with no protein the body can't make new antibodies. Immunocompromised patients (e.g. AIDS) — immune system itself is damaged ("front-line soldiers bought by the enemy") → no response to any number of vaccines. |
| 2. Live vaccines | the attenuated / weakened pathogen can mutate / reverse inside the body → regains disease-causing ability → causes the disease. |
| 3. Antigenic variation | mutation changes the antigen so the vaccine no longer matches (why flu and COVID are hard to vaccinate against). Antigenic drift = minor changes (people slowly drifting apart). Antigenic shift = major change (shifting house). |
| 4. Antigenic concealment | pathogen hides inside body cells (e.g. liver cells; malaria — later), not in blood → WBCs/antibodies never see it → no immune response. |
Careful: Malnourished ≠ "zero antibodies". Sir: the problem is that
new antibodies are not produced in response to the vaccine.
12. Primary & Secondary Immune Response
Primary immune response: the response generated on first exposure to an
antigen.
Secondary immune response: the response on second or subsequent
exposure to the same antigen.
| Primary immune response | Secondary immune response |
|---|---|
| (a) Slow — due to lack of memory cells (longer lag phase) | (a) Rapid / quick — memory cells recognise antigen at once |
| (b) Peak antibody conc. is not as high as the secondary response | (b) Peak antibody concentration is higher |
| (c) Antibodies stay in blood for a shorter time — hydrolysed within the body (rapid decline) | (c) Antibodies stay in blood for a longer time |
★ Exam Tip: Graph questions: describe lag time, rate of rise, peak
height and how fast it falls for both. Cause of the difference = memory cells (B memory → plasma
cells quickly).
13. Monoclonal Antibodies (MABs)
mono = single · clone = identical / similar cells. Each antibody is specific for one antigen. MABs = antibodies against a particular antigen produced by hybridoma cells.
Plasma cell(1) makes large amounts of identical
antibodies
(2) short-lived, cannot divide by mitosis
(2) short-lived, cannot divide by mitosis
Myeloma cell (cancerous B cell)(1) long-lived, divides by mitosis
(2) cannot produce / release antibodies
(2) cannot produce / release antibodies
Production of monoclonal antibodies
- Insert the pathogen (antigen) into a rabbit / mouse.
- Allow sufficient time for the immune response to produce plasma cells against the antigen.
- Extract the plasma cells from the spleen of the rabbit / mouse.
- Fuse plasma cell with myeloma cell in the presence of fusogen → hybridoma cell.
- Select the clone of desired hybridoma cells producing the desired antibodies.
- Culture the selected clone in large fermenters.
- Isolate the antibodies.
- Humanisation of the antibodies takes place (so humans don't reject mouse antibodies).
Uses of MABs
| Diagnostic | Therapeutic / treatment |
|---|---|
| (1) Diagnose DVT (deep vein thrombosis = clot): anti-fibrin antibody (binds the clot)
tagged with gamma radiation → the clot's location is detected • identify the location of tumours • identification of pathogens |
(1) Trastuzumab — a specific kind of breast cancer (2) Ipilimumab — against a certain type of skin cancer (3) Infliximab — to manage rheumatoid arthritis |
Note: The board's diagnostic list was cut off after "identify the
location of tumours" and "identification of pathogens" — add any other diagnostic uses from your
syllabus/textbook.
✓ Quick Recap — Whole Chapter (1/2)
- Pathogen = organism · pathogenicity = ability · antigen = macromolecule (cell recognition marker) · self = no response, non-self = response.
- Leukocytes: phagocytes (neutrophils, monocytes → macrophages) · lymphocytes (B: plasma + memory; T: helper + killer + memory). Granulocytes (granules + lobed nucleus) vs agranulocytes (large spherical nucleus in lymphocytes).
- Defence: ① external (skin, nasal hair | mucus, HCl | platelets) non-specific, no WBCs → ② innate (phagocytes, non-specific, no memory) → ③ adaptive (lymphocytes, specific, memory).
- Phagocytosis: chemotaxis → recognition + attachment → endocytosis (phagosome) → lysosome fuses (phagolysosome) → hydrolytic enzymes digest → exocytosis. Fails → antigen presentation by macrophage (APC).
- Stem cells (bone marrow): myeloid → all other blood cells · lymphoid → B & T. T mature in thymus, B in bone marrow. Receptors added at maturation; B receptor = antibody.
- Antibody: glycoprotein, globular, 4 chains (2 light + 2 heavy), quaternary, 16 S–S bonds · variable region = antigen-binding · constant region = same for all, helps phagocytosis.
- Functions: opsonisation · block viruses · antitoxins · stop flagella · punch holes → lysis · agglutination.
- Humoral: APC → TH binds → mitosis (½ TH memory) → cytokines → clonal selection of B clone → clonal expansion → differentiation: plasma cells (antibodies) + B memory (lymph nodes).
- Cell-mediated: virus-infected / tumour cells → TH cytokines → TK clone selected & expanded → activated TK (H₂O₂ + interferons punch holes → lysis) + TK memory.
✓ Quick Recap — continued
- Immunity types: active (natural / artificial = vaccination, long-term) · passive (placenta, breast milk / injected antibodies, short-term).
- Vaccines: killed · live (attenuated) · subunit/toxoid · genetically engineered. Good vaccine = low toxicity, both responses, thermostable, cheap, all ages/ethnicities, no booster. Problems: poor response (malnourished / immunocompromised), live reversal, antigenic variation (drift minor / shift major), antigenic concealment.
- Primary = slow, lower peak, short-lived AB · secondary = rapid, higher peak, long-lasting (memory cells).
- MABs: plasma cell (spleen of immunised mouse) + myeloma cell + fusogen → hybridoma → select clone → ferment → isolate → humanise. Uses: DVT (anti-fibrin + γ), tumour location, pathogen ID · trastuzumab, ipilimumab, infliximab.