Antigens and Phagocytosis — AQA A-level Biology

SPEC 3.2.4 - CELLS — IMMUNITY

Cell Recognition & the Immune System

Antigens · Phagocytosis · Cellular response (T cells) · Humoral response (B cells) · Antibodies · Vaccines · Active & passive immunity

The Immune System — Overview

The immune system has two levels of defence that operate together to protect the body from pathogens.

Non-specific Defences (First Line)

Skin — physical barrier; sebum is acidic

Mucus — traps pathogens in airways

Cilia — sweep mucus and trapped pathogens away from lungs

Phagocytosis — engulfs and destroys any foreign particle; not antigen-specific

Acts immediately; does not require prior exposure

Specific Immune Response (Second Line)

Targets specific antigens

Cellular response — T lymphocytes; destroys infected cells

Humoral response — B lymphocytes; produces antibodies

Takes days to develop on first exposure

Produces immunological memory

Definition — Antigen

An antigen is a molecule (usually a protein or glycoprotein) on the surface of a cell or pathogen that is recognised as foreign by the immune system and stimulates an immune response.

Cell Recognition — Self vs Non-self

Every cell carries surface molecules that act as identity markers. The immune system uses these to distinguish what belongs to the body from what does not.

What the Immune System Identifies

CategoryExamplesResponsePathogensBacteria, viruses, fungiAttacked and destroyedCells from other organisms of same speciesTransplanted organs, transfused blood (wrong type)Attacked — transplant rejectionAbnormal body cellsCancer cells, virus-infected cellsDestroyed by cytotoxic T cellsToxinsBacterial exotoxinsTrigger immune response

Surface Glycoproteins — The Identity Molecules

Each cell type carries specific glycoproteins on its surface. These act as antigens when introduced into a different individual. The immune system learns to tolerate "self" glycoproteins — any glycoprotein it does not recognise as self is treated as an antigen and triggers a response.

Synoptic Link — Transplants

Organ transplant rejection occurs because donor glycoproteins are recognised as non-self antigens by the recipient's immune system. Immunosuppressant drugs (e.g. cyclosporin) reduce this response, but leave the patient vulnerable to infection.

Antigen Variability & Disease Prevention

Pathogens — particularly viruses — can change their surface antigens through mutation. This has major consequences for immunity and vaccine effectiveness.

Why Antigen Variability Matters

Memory cells from a previous infection are specific to the original antigen

If the pathogen mutates its surface antigens (antigenic variation), existing memory cells no longer recognise it

The immune system must mount a primary response — slower and weaker — against the new variant

This is why influenza vaccines must be reformulated each year

HIV mutates its surface proteins rapidly — makes vaccine development extremely difficult

Examiner Alert ⚠️

A common error is to say "the pathogen becomes immune to antibodies." Pathogens do not become immune. The correct explanation is: mutations change the pathogen's surface antigens, so existing antibodies and memory cells no longer have a complementary binding site — they cannot recognise and bind to the new antigen shape.

Phagocytosis

Definition — Phagocytosis

Phagocytosis is the engulfment and digestion of pathogens or cellular debris by phagocytes (neutrophils and macrophages).

1

Phagocyte detects chemical signals released by pathogens or damaged tissue (chemotaxis) and moves toward the pathogen

2

Phagocyte's cell-surface receptors bind to antigens on the pathogen's surface; the plasma membrane extends around the pathogen (pseudopodia formation)

3

The pathogen is engulfed into a membrane-bound vesicle called a phagosome

4

A lysosome fuses with the phagosome → forms a phagolysosome

5

Lysozymes (hydrolytic enzymes) in the lysosome digest and destroy the pathogen; the phagocyte may then present antigens on its surface

Examiner Alert ⚠️

Distinguish carefully: a lysosome is an organelle containing digestive enzymes; a lysozyme is the enzyme inside it. These terms are frequently confused in exams. Also note: it is lysozymes (enzymes) that digest the pathogen — not the lysosome itself.

Antigen-Presenting Cells

After phagocytosis, some phagocytes (particularly macrophages) do not simply destroy the antigen — they display fragments of it on their surface. This is the critical link between non-specific and specific immunity.

Definition — Antigen-Presenting Cell (APC)

An antigen-presenting cell (APC) is a cell (usually a macrophage) that displays foreign antigens on its surface after phagocytosis, thereby stimulating T lymphocytes to initiate the specific immune response.

How APCs Link Phagocytosis to Specific Immunity

Macrophage engulfs and partially digests pathogen by phagocytosis

Fragments of the pathogen's antigens are displayed on the macrophage's outer surface

The macrophage is now an APC — it carries the "wanted poster" for T cells to read

A helper T cell with a complementary receptor binds to the displayed antigen → T cell is activated

Exam Tip

AQA mark schemes require you to say the antigen is "displayed on the surface" of the APC — not simply that the macrophage "shows" the antigen. The word "surface" is a specific marking point that students frequently omit.

The Cellular Immune Response — T Lymphocytes

1

APC displays foreign antigen on its surface; a helper T cell (T_H cell) with a complementary receptor binds to the antigen

2

The helper T cell undergoes clonal selection (the right cell is selected) and clonal expansion (divides by mitosis to form a large clone of identical T_H cells)

cytokines

Cytotoxic T cells (T_C cells) → kill infected body cells

B cells → produce antibodies (humoral response)

Phagocytes → become more active

4

Cytotoxic T cells recognise infected body cells (which display pathogen antigens on their surface) and destroy them. They do this by making direct contact with the infected cell and causing cell lysis — killing the infected cell and the pathogen inside it

5

Some T cells become memory T cells — long-lived cells that persist after the infection and enable a faster response on re-exposure

Cellular Response — Summary Diagram

The Humoral Immune Response — B Lymphocytes

The humoral response involves B lymphocytes producing antibodies that circulate in the blood and lymph. It is activated when a B cell with a complementary receptor binds to its specific antigen, and is also assisted by cytokines from helper T cells.

1

A B cell with a complementary receptor binds to the free antigen; cytokines from T_H cells also stimulate the B cell

2

Clonal selection: the specific B cell is selected by its antigen. Clonal expansion: it divides by mitosis to produce a large clone of identical B cells

Plasma cells — short-lived; secrete thousands of antibodies per second into blood/lymph

Memory B cells — long-lived; persist in the body for years; enable rapid secondary response

4

Antibodies bind to antigens on pathogens forming antigen-antibody complexes → leads to destruction of the pathogen

Examiner Alert ⚠️

It is plasma cells that secrete antibodies — NOT B cells directly. B cells differentiate INTO plasma cells first. A very common error is to say "B cells release antibodies." The correct sequence is: B cell → clonal expansion → plasma cell → antibody secretion.

Antibody Structure

Definition — Antibody

An antibody is a protein (immunoglobulin) with a specific antigen-binding site complementary to one antigen; it consists of four polypeptide chains (two heavy and two light) joined by disulfide bonds, with a variable region forming the antigen-binding site.

Antigen-Antibody Complex & Destruction

Antibodies destroy pathogens by binding to their antigens and forming antigen-antibody complexes. AQA specifies two mechanisms of destruction students must know:

Agglutination

Because each antibody has two antigen-binding sites, it can cross-link multiple pathogen cells simultaneously. This causes pathogens to clump together (agglutinate), which:

Slows pathogen movement

Makes them much easier for phagocytes to engulf (larger target)

Prevents pathogens from binding to host cells

Phagocytosis of Bacterial Cells

Antibodies bind to antigens on the surface of pathogens, forming antigen-antibody complexes. This makes it easier for phagocytes to engulf and destroy the pathogens. The antibody acts as a signal that marks the pathogen for destruction by phagocytosis.

Antibodies act as a "flag" marking the pathogen for destruction

Greatly increases rate of phagocytosis

AQA Specification Note

AQA only requires knowledge of agglutination and phagocytosis as mechanisms by which antigen-antibody complexes lead to destruction of antigens. You do not need to know about complement activation or antibody-dependent cellular cytotoxicity for this specification.

Primary & Secondary Immune Responses

FeaturePrimary ResponseSecondary Response

TriggerFirst exposure to antigenRe-exposure to same antigen

SpeedSlow — 7–14 days to peak antibody levelFast — 1–3 days to peak

Antibody levelLow peak; falls rapidlyMuch higher peak; maintained longer

Cause of differencePrimary: naive lymphocytes; slow clonal expansion from small numbersLarge population of memory cells already exists; rapid clonal expansion

SymptomsDisease symptoms usually appearOften no symptoms — infection cleared before it develops

Why the Secondary Response is Faster and Stronger

During the primary response, memory B cells and memory T cells are produced alongside plasma cells and effector T cells. Memory cells are long-lived, carry the specific receptor for the original antigen, and persist for years or decades. On re-exposure, they divide rapidly — clonal expansion from a large starting population — producing high antibody levels within days, before the infection can cause symptoms.

Vaccines & Herd Immunity

Vaccines exploit the immunological memory mechanism to provide protection without causing disease.

How Vaccines Work

Contain antigen from the pathogen (killed/weakened organism, purified protein subunit, or toxoid)

Antigen is not pathogenic — does not cause disease

Triggers a primary immune response and production of memory cells

On subsequent exposure to the real pathogen: rapid secondary response destroys it before symptoms develop

Herd Immunity

If a sufficiently large proportion of a population is immune to a pathogen, the chain of transmission is broken — even unvaccinated individuals gain indirect protection because they are unlikely to encounter an infected person. The proportion required varies by how infectious the pathogen is.

Examiner Alert ⚠️

Students often confuse active and passive immunity when discussing vaccines. Vaccines produce active immunity — the individual's own immune system responds and produces memory cells. This provides long-term protection. Do not confuse this with passive immunity (transferred antibodies, no memory cells, short-term).

Active & Passive Immunity

FeatureActive ImmunityPassive Immunity

How antibodies ariseIndividual's own plasma cells produce themReady-made antibodies transferred from another organism

Memory cellsYes — produced; long-term protectionNo — no memory cells; temporary protection only

DurationLong-term (years to lifelong)Short-term (weeks to months — until antibodies degrade)

SpeedSlower — takes days to weeks to developImmediate — antibodies already present

Natural examplesSurviving infection (e.g. chickenpox)Placental transfer of maternal IgG to foetus; colostrum (breast milk)

Artificial examplesVaccinationInjection of antiserum/antivenom (e.g. snakebite)

Synoptic Link — Why Passive Immunity is Short-term

Transferred antibodies are proteins — they are eventually broken down by the recipient's own proteases. Without memory cells, there is no mechanism to produce more of those specific antibodies. This is why newborns become susceptible to infection as maternal antibodies degrade over the first months of life.

DEEP Chain — Cellular Response (Extended Answer)

"Describe and explain the cellular immune response to a bacterial infection." [6 marks]

DEEP Chain

DDefine: The cellular immune response involves T lymphocytes and targets infected body cells and pathogens displaying non-self antigens on their surface.

EExplain mechanism: A macrophage engulfs the bacterium by phagocytosis and becomes an antigen-presenting cell, displaying the bacterial antigen on its surface. A helper T cell (T_H) with a complementary receptor binds to this antigen, undergoes clonal selection and expansion by mitosis, and releases cytokines.

EEvidence/named detail: Cytokines stimulate cytotoxic T cells (T_C) to divide and become active. T_C cells recognise infected body cells displaying the bacterial antigen, bind to them, and cause cell lysis — killing the infected cell and the pathogen replicating inside it.

PPractical/application: Some T cells from the clone differentiate into long-lived memory T cells. On re-exposure to the same bacterium, memory T cells enable rapid clonal expansion — a faster, stronger secondary response that clears the infection before symptoms develop.

Practice Question 1

A patient receives a kidney transplant from a donor. Despite taking immunosuppressant drugs, the patient's body begins to reject the transplanted kidney.

(a) Explain why the patient's immune system attacks the transplanted kidney. [3 marks]

(b) Explain why immunosuppressant drugs increase the patient's risk of infection. [2 marks]

D:

The donor kidney cells carry glycoproteins (antigens) on their surface that are different from the recipient's own glycoproteins — they are recognised as non-self. [1]

E:

The recipient's helper T cells bind to these foreign antigens (displayed on antigen-presenting cells) and undergo clonal expansion. Cytokines stimulate cytotoxic T cells, which attack and destroy the transplanted kidney cells displaying non-self antigens. [2]

E (b):

Immunosuppressant drugs reduce the activity of T lymphocytes and other immune cells. This suppresses the rejection response but also impairs the immune system's ability to respond to pathogens — both the cellular and humoral responses are weakened, so infections that would normally be cleared rapidly can become life-threatening. [2]

Practice Question 2

A child is vaccinated against measles at 12 months old. At age 7, they are exposed to the measles virus at school but do not develop the disease.

(a) Explain why the child does not develop measles after exposure at age 7. [4 marks]

(b) Explain the difference between active and passive immunity, giving one example of each. [4 marks]

D:

The vaccine introduced measles antigens and triggered a primary immune response — clonal expansion of B cells with complementary receptors, producing plasma cells and memory B cells. [1]

E:

Memory B cells (and memory T cells) persist in the body for years after vaccination. On re-exposure to measles virus at age 7, these memory cells are rapidly activated. [1]

E:

Memory cells undergo rapid clonal expansion — producing large numbers of plasma cells quickly. A high level of antibody is produced within 1–3 days (secondary response) — much faster than the primary response. [1]

P:

Antibodies bind to measles virus antigens, causing agglutination and promoting phagocytosis, clearing the virus before it can replicate sufficiently to cause disease symptoms. [1]

D (b):

Active immunity: the individual's own immune system produces antibodies in response to antigen; memory cells are formed; protection is long-term. Example: vaccination against measles OR natural infection with chickenpox. [2]

E (b):

Passive immunity: ready-made antibodies are transferred into the individual from an external source; no memory cells are produced; protection is short-term. Example: transfer of IgG antibodies across the placenta from mother to foetus OR injection of antivenom after snakebite. [2]

Summary

Key Points — Spec 3.2.4

TopicWhat to Know

Cell recognitionGlycoproteins on surfaces identify cells; immune system recognises pathogens, foreign cells, abnormal cells, toxins

Antigen variabilityMutations change surface antigens → memory cells no longer complementary → primary response required again

PhagocytosisPhagosome + lysosome → phagolysosome → lysozymes digest pathogen; macrophage → APC

Cellular responseAPC → T_H cell activated → clonal expansion → cytokines → T_C cells (destroy infected cells), B cells, phagocytes stimulated

Humoral responseB cell → clonal selection/expansion → plasma cells (antibodies) + memory B cells

Antibody structureY-shaped; 2 heavy + 2 light chains; variable region = antigen-binding site; 2 binding sites per antibody

Antibody actionAgglutination (antibodies cross-link pathogens → clumps → easier phagocytosis) + phagocytosis of bacterial cells

Primary vs secondarySecondary: faster, higher antibody level, due to memory cells

Active immunityOwn antibodies; memory cells; long-term; vaccination or natural infection

Passive immunityTransferred antibodies; no memory cells; short-term; placenta/colostrum/antiserum

Top 3 Examiner Errors

1. Saying "B cells release antibodies" — it is plasma cells (differentiated B cells) that secrete antibodies.

2. Confusing lysosome (organelle) with lysozyme (enzyme).

3. Saying helper T cells kill pathogens — T_H cells coordinate the response; T_C cells kill infected body cells.