IB Biology HLDisease & ImmunityPaper 1 & 2~13 min read
The Adaptive Immune Response
This is the long chain of events that turns “something foreign is here” into a blood full of antibodies aimed at exactly that thing. Learn it as a story with an order, not as a list of cells, and it stops being intimidating.
📘 What you need to know
Cells carry unique molecules on the surface membrane that act as markers, allowing cell–to–cell recognition. Some glycolipids and glycoproteins act as antigens.
Antigens are found on bacterial cell walls, virus envelopes, cancer cells and even pollen grains.
Red blood cells carry antigens that determine blood group: the ABO marker and the Rhesus (Rh) marker.
An incompatible transfusion causes agglutination — red blood cells clumping together — which can be fatal.
A phagocyte that has engulfed a pathogen displays its antigens, becoming an antigen–presenting cell.
A T helper cell with the complementary receptor binds and becomes activated, then releases signalling proteins that activate the matching B cell.
Clonal expansion: the activated B cell divides by mitosis to produce plasma cells (which secrete antibodies) and memory cells.
The secondary response is faster and larger than the primary response, so the pathogen is destroyed before symptoms develop.
Antigens: the name badges
Every organism has cells with unique molecules on the cell surface membrane that act as markers to identify it. These markers are macromolecules, and they allow cell–to–cell recognition.
Your immune system uses them to sort everything into self and non–self. Anything with non–self markers triggers a response, and molecules that do this are called antigens.
Antigens appear on the cell surface membranes of cancer cells, on bacterial cell walls, in the envelopes of viruses, and on pollen grains.
Some glycolipids and glycoproteins on the outer surface of the membrane act as antigens.
Allergies are an immune response triggered by antigens on the surface of an allergen, such as pollen. There is no pathogen involved.
Antigens on red blood cells
Red blood cells carry their own set of surface antigens, and those antigens decide your blood group. Two markers matter:
The ABO marker, which decides whether you are group A, B, AB or O.
The Rhesus (Rh) marker, which decides whether you are Rh positive or Rh negative.
All four ABO groups start from the same base structure, an ‘H’ marker. What differs is the molecule attached to it:
Blood group
What is attached to the H marker
Antigens on the red blood cells
Can safely receive from
A
N–acetylgalactosamine
Type A antigen
A and O
B
Galactose
Type B antigen
B and O
AB
Two H markers — one with N–acetylgalactosamine, one with galactose
Type A and type B antigens
A, B, AB and O — the universal recipient
O
Nothing — the H marker is not modified
Neither A nor B antigens
O only, but can donate to everyone
Universal donor, universal recipient. Group O negative has no A, no B and no Rhesus antigen, so there is nothing for a recipient’s antibodies to attack — it can be given to anyone. Group AB positive has all three antigens, so it treats every donor blood type as self and can receive from anyone.
If a transfusion is given to someone with an incompatible blood type, antibodies already present in the recipient’s blood bind to the donor cells because those cells carry non–self antigens. The result is agglutination: red blood cells clumping together in the blood vessels. This can be fatal, which is why blood must be matched before transfusion.
Blood groups are the cleanest example of self and non–self in the whole topic. Nothing here is a pathogen. The donor cells are perfectly healthy human cells — they are simply wearing the wrong name badge for that recipient.
How a B cell gets activated
B cells cannot switch themselves on. Getting one activated takes three cells working in order, and questions on this almost always want the sequence.
Step 3 is the one students leave out. A B cell that has bound its antigen is still not switched on until a T helper cell tells it to be.
🧩 The activation sequence in words
A phagocyte engulfs a pathogen and presents the pathogen’s antigens on its own cell surface membrane. A cell doing this is an antigen–presenting cell.
The T helper cell with the complementary receptor proteins binds to that antigen and becomes activated.
The activated T helper cell binds to complementary receptors on the surface of the specific B lymphocyte and releases signalling proteins.
The B cell — which has already bound its antigen, forming an antigen–antibody complex — is now activated.
The activated B cell undergoes clonal expansion: it divides repeatedly by mitosis, making many identical clones, each producing the exact same antibody.
Some clones become plasma cells, which secrete antibodies. Others become memory cells, which remain circulating in the blood.
Plasma cells and memory cells
Plasma cells
Memory cells
Job
Secrete specific antibodies against the non–self antigen
Stay in the blood ready for a future infection
How long they matter
The antibodies they make last weeks or months
The cells can last many years, often a lifetime
What they give you
The response to the infection happening now
Immunological memory — a fast response next time
Primary and secondary responses
Immunity begins when exposure to a specific antigen produces complementary antibodies and memory cells. That first exposure triggers the primary immune response, and immunity develops if memory cells and antibodies persist after the pathogen has been cleared.
When the same antigen turns up again, the secondary immune response runs. Memory cells recognise the antigen, divide very quickly, and differentiate into antibody–producing plasma cells and yet more memory cells.
The response to a pathogen you have met before is extremely fast, so the infection is destroyed and removed before the pathogen population grows enough to cause symptoms.
Why you only get measles once, but colds forever. There is essentially one strain of the measles virus, so your memory cells recognise it every time and you never feel ill again. Colds and influenza are caused by viruses that constantly develop new strains, and each strain carries different antigens, so a slow primary response has to run all over again.
Worked examples
WE 1
Describe the activation of a B lymphocyte
Describe how a B lymphocyte is activated following infection by a bacterium. (4 marks)
Point 1: presentation
A phagocyte engulfs the bacterium and displays its antigens on its own surface membrane, becoming an antigen–presenting cell.
Point 2: the T helper
A T helper cell with complementary receptor proteins binds to that antigen and becomes activated.
Point 3: the signal
The activated T helper cell binds to the specific B cell and releases signalling proteins.
Point 4: activation
The B cell has also bound the antigen with its antibody receptor, forming an antigen–antibody complex, and this combination activates it.
Present, bind, signal, activate — the B cell needs both inputsthe word “complementary” is doing real work here — only the matching cells respond
WE 2
Compare the primary and secondary responses
Using the graph above, compare the primary and secondary immune responses. (3 marks)
Point 1: size
The secondary response reaches a much higher concentration of antibodies than the primary response.
Point 2: speed
It also rises far more steeply and peaks sooner after exposure, within about a week rather than around three weeks.
Point 3: the reason
Memory cells left over from the primary response recognise the antigen immediately and divide rapidly into plasma cells, so antibodies are produced without the delay of a first encounter.
Bigger, faster, and it is memory cells that make the differenceuse figures from the axes if the graph gives them — “much higher” alone can lose a mark
WE 3
Explain the danger of an incompatible transfusion
Explain why giving group A blood to a patient with group B blood is dangerous. (3 marks)
Point 1: the antigens
Group A red blood cells carry the type A antigen, which is non–self to a group B patient.
Point 2: the response
Antibodies already present in the recipient’s plasma bind to those non–self antigens on the donated cells.
Point 3: the consequence
The red blood cells clump together, which is agglutination, and this can block blood vessels and be fatal.
Non–self antigen, antibodies bind, agglutination in the vesselsuse the word agglutination — “the blood goes lumpy” will not score
💡 Exam tips
Learn the order and name every cell: phagocyte → antigen–presenting cell → T helper → B cell → plasma and memory cells.
Say the T helper releases signalling proteins and that the receptors are complementary.
Use clonal expansion and say the clones make the exact same antibody.
For graph questions, describe both the size and the speed of the secondary response.
Say plasma cells secrete antibodies and memory cells remain in the blood.
For blood groups, always explain danger in terms of non–self antigens and agglutination.
⚠ Common mistakes
Saying B cells make antibodies. They divide into plasma cells, and those secrete the antibodies.
Leaving out the T helper cell. Antigen binding alone does not activate a B cell.
Saying memory cells make antibodies immediately. They divide and differentiate into plasma cells first — it is just very fast.
Mixing up antigen and antibody in the complex. It is an antigen–antibody complex, formed when a receptor binds its antigen.
Saying group O has no blood group. It has the unmodified H marker — just no A or B antigens.
Claiming immunity to flu is impossible. You do become immune to a strain; the virus keeps producing new ones with different antigens.
Up next: HIV & AIDS. You now know that T helper cells are the switch for the whole adaptive response. The next page looks at a virus that destroys exactly that cell, and why that is so devastating.
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