How does the immune system defend the body against pathogens?
Antigens and the difference between the cellular and humoral immune responses, the action of B and T lymphocytes, antibodies and immunological memory, and active and passive immunity and vaccination.
A CCEA A-Level Biology answer on antigens and the cellular and humoral immune responses, the action of B and T lymphocytes, antibodies and immunological memory, and active and passive immunity and vaccination.
Reviewed by: AI editorial process; not yet individually human-reviewed
Have a quick question? Jump to the Q&A page
Jump to a section
What this dot point is asking
CCEA wants you to explain what antigens are, distinguish the cellular and humoral immune responses, describe the action of B and T lymphocytes and antibodies, explain immunological memory, and distinguish active from passive immunity and the role of vaccination.
Antigens and the immune responses
Before the specific response, phagocytes (such as macrophages) engulf and digest pathogens by phagocytosis, then display the pathogen's antigens on their surface as antigen-presenting cells, which kick-starts the specific response.
Lymphocytes and antibodies
Antibodies work in several ways: they agglutinate (clump) pathogens so phagocytes engulf many at once, they act as opsonins that label pathogens for destruction, and some neutralise toxins (antitoxins). The variable region differs between antibodies, giving each one its specificity, while the constant region is the same.
Immunity and vaccination
Memory cells remain after an infection and give a faster, stronger secondary response if the same antigen returns (immunological memory). Active immunity is made by your own body after infection or vaccination, takes time to develop, but is long-lasting because memory cells form; passive immunity is from ready-made antibodies (for example across the placenta, in breast milk or in an injection) and is immediate but short-lived because no memory cells form. Vaccination introduces harmless antigens (dead, attenuated or fragments) so memory cells form without illness, and widespread vaccination gives herd immunity, protecting those who cannot be vaccinated by reducing the spread of the pathogen.
Examples in context
Example 1. Why measles vaccination protects whole communities. Measles is highly infectious, so herd immunity needs about 95 percent of people vaccinated. When uptake falls, the proportion of susceptible people rises and outbreaks occur, harming infants too young to be vaccinated and those who cannot be (for medical reasons). This shows how active immunity in individuals, through vaccination producing memory cells, scales up to protect a population.
Example 2. Antibodies across the placenta in newborns. A newborn receives maternal antibodies across the placenta and in breast milk, giving passive immunity to diseases the mother is immune to. This protection fades over a few months as the antibodies are broken down and no memory cells were made by the baby. It explains why infants are vaccinated to build their own active immunity once maternal protection wanes.
Try this
Q1. Explain why the secondary immune response is faster and stronger than the primary response. [2 marks]
- Cue. Memory cells from the first exposure divide rapidly into plasma cells, producing antibodies sooner and in greater quantity.
Q2. State one difference between active and passive immunity. [1 mark]
- Cue. Active immunity is made by the body and lasts long; passive immunity is received ready-made and is short-lived.
Q3. Suggest why a person can catch a cold many times but usually catches measles only once. [3 marks]
- Cue. Cold viruses exist as many different strains with different antigens, so memory cells do not recognise new strains; measles has stable antigens, so memory cells give lasting protection after one infection or vaccination.
Exam-style practice questions
Practice questions written in the style of CCEA exam questions on this dot point, with worked answer explainers. The year tag is the paper they imitate, not the source.
CCEA 20196 marksDescribe the roles of B lymphocytes and T lymphocytes in the immune response to a bacterial infection.Show worked answer →
A 6-mark answer needs the cellular and humoral responses with named cell types and their actions.
Antigen presentation: a macrophage engulfs the pathogen and displays its antigens on its surface (an antigen-presenting cell).
T helper cells: have receptors complementary to the antigen, are selected and activated, and release chemicals (cytokines) that stimulate B cells and other T cells (clonal selection).
T killer (cytotoxic) cells: destroy body cells that display the foreign antigen, important against intracellular pathogens.
B lymphocytes: the B cell with the complementary antibody is selected and divides by mitosis (clonal expansion) into plasma cells and memory cells.
Plasma cells: secrete large numbers of specific antibodies that bind the antigen and agglutinate the pathogen, marking it for phagocytosis.
Memory cells: remain to give a faster secondary response.
Markers reward antigen presentation, T helper activation, B cell selection, plasma cell antibody production, and memory cells.
CCEA 20215 marksExplain the difference between active and passive immunity, and explain why a vaccine gives long-lasting protection while an injection of antibodies does not.Show worked answer →
A 5-mark answer needs both definitions and the link to memory cells.
Active immunity: the body is exposed to an antigen (by infection or vaccination) and makes its own antibodies and, importantly, memory cells. It takes time to develop but is long-lasting.
Passive immunity: the body receives ready-made antibodies (for example across the placenta, in breast milk, or by injection of antitoxin). It is immediate but short-lived because no memory cells are formed and the antibodies are broken down.
Why a vaccine lasts: vaccination triggers an active response that produces memory cells. On later exposure to the real pathogen, these memory cells give a rapid, large secondary response before symptoms develop.
Why injected antibodies do not last: no memory cells are made, and the introduced antibodies are gradually degraded, so protection ends within weeks.
Markers reward both definitions, the role of memory cells, and the contrast in duration.
Related dot points
- Genes, alleles and genotypes, monohybrid and dihybrid inheritance, sex linkage, codominance, and the use of genetic diagrams and the chi-squared test.
A CCEA A-Level Biology answer on genes, alleles and genotypes, monohybrid and dihybrid inheritance, sex linkage and codominance, and the use of genetic diagrams and the chi-squared test.
- Recombinant DNA technology and genetic engineering, the polymerase chain reaction, gel electrophoresis and DNA profiling, and the applications and ethics of gene technology.
A CCEA A-Level Biology answer on recombinant DNA technology and genetic engineering, the polymerase chain reaction, gel electrophoresis and DNA profiling, and the applications and ethics of gene technology.
- Ecosystems, energy flow and food webs, the carbon and nitrogen cycles, succession, and the principles of conservation and managing human impact.
A CCEA A-Level Biology answer on ecosystems, energy flow and food webs, the carbon and nitrogen cycles, succession, and the principles of conservation and managing human impact.
- Natural selection and the sources of variation, the Hardy-Weinberg principle and allele frequencies, types of selection, and the mechanisms of speciation.
A CCEA A-Level Biology answer on natural selection and the sources of variation, the Hardy-Weinberg principle and allele frequencies, types of selection, and the mechanisms of speciation.
- The structure of viruses, why they are non-cellular, the lytic and lysogenic cycles, the replication of HIV as a retrovirus, and how viruses cause disease.
A CCEA A-Level Biology answer on the structure of viruses, why they are non-cellular, the lytic and lysogenic replication cycles, the replication of HIV as a retrovirus, and how viruses cause disease.
Sources & how we know this
- CCEA GCE Biology specification — CCEA (2016)