Adaptive immune response: Humoral and cell-mediated immunity - TCE Biology (Tasmania)
“The third line of defence is adaptive and specific: persistent adaptive responses to specific antigens, including humoral immunity through the production of antibodies by B lymphocytes and cell-mediated immunity provided by T lymphocytes, with memory cells giving long-term immunity; the roles of antigen-presenting cells (dendritic cells and macrophages), mast cells, neutrophils, B lymphocytes, memory B cells, T lymphocytes, helper T cells, cytotoxic T cells, regulatory T cells and memory T cells”
The adaptive (third line) response targets specific antigens and produces memory. Antigen-presenting cells (dendritic cells and macrophages) show a pathogen's antigens to helper T cells, which activate the rest of the response. In humoral immunity, B lymphocytes with matching receptors multiply into plasma cells, which make antibodies that bind the antigen, and memory B cells. In cell-mediated immunity, cytotoxic T cells destroy infected body cells, memory T cells remain, and regulatory T cells switch the response off. Memory cells make a second response faster and stronger, giving long-term immunity.
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What this dot point is asking
The adaptive response is part of criterion 7 (Section D of the TASC exam). The external assessment specifications include the humoral response (B lymphocytes, plasma B cells, memory B cells, antibodies with antigen-binding sites specific to the pathogen) and the cell-mediated response (T lymphocytes, helper, cytotoxic, memory and regulatory T cells). Antibody classes (IgG and others), heavy and light chains, the allergic response and the terms MHC I and MHC II are excluded.
Key terms
- Antigen: a molecule, usually on the surface of a pathogen or infected cell, that the immune system recognises as non-self and responds to.
- Receptor: a protein on the surface of a B or T cell with a shape complementary to one specific antigen.
- Antibody: a Y-shaped protein made by plasma cells, with antigen-binding sites complementary to one specific antigen.
TASC's 2025 assessment report noted that candidates commonly confused receptors, antigens and antibodies, so learn these definitions exactly.
Starting the response: antigen presentation
Dendritic cells and macrophages engulf pathogens (see the innate immune response) and display the pathogen's antigens on their surface. In lymph nodes they present the antigen to helper T cells. Only helper T cells whose receptors are complementary to that antigen are activated. Activated helper T cells multiply and release chemical signals that activate B cells and cytotoxic T cells.
Humoral immunity (B lymphocytes and antibodies)
- A B lymphocyte whose receptors match the antigen binds to it.
- With signals from an activated helper T cell, the B cell divides rapidly to form a clone (clonal selection and expansion).
- Most clones become plasma cells, which secrete large amounts of antibodies specific to the antigen.
- Some become memory B cells, which remain in the body for years.
What antibodies do: they bind to antigens on pathogens or toxins, neutralising them (blocking viruses from entering cells and toxins from acting), clumping pathogens together, and marking them for destruction by phagocytes. Humoral immunity mainly targets pathogens and toxins outside cells, in blood and tissue fluid.
Cell-mediated immunity (T lymphocytes)
- An antigen-presenting cell activates a matching helper T cell.
- The helper T cell releases signals that activate cytotoxic T cells with receptors complementary to the same antigen, and they multiply.
- Cytotoxic T cells bind to body cells displaying the antigen (infected or abnormal cells) and destroy them, which stops viruses and other pathogens that live inside cells from replicating.
- Memory T cells remain for long-term immunity.
- Regulatory T cells suppress the response once the pathogen is under control, preventing damage to healthy tissue.
Humoral: B cells and antibodies, against pathogens and toxins in body fluids. Cell-mediated: cytotoxic T cells, against infected body cells. Helper T cells are needed for both.
Summary of cells
| Cell | Line | Role |
|---|---|---|
| Neutrophil | Second | Phagocyte; first to arrive at infection (not an antigen-presenting cell) |
| Mast cell | Second | Releases histamine to start inflammation |
| Macrophage | Second, links to third | Phagocyte; antigen-presenting cell |
| Dendritic cell | Second, links to third | Phagocyte; main antigen-presenting cell for T cells |
| B lymphocyte | Third | Recognises antigen; becomes plasma cells (antibodies) and memory B cells |
| Memory B cell | Third | Long-lived; rapid antibody response on re-exposure |
| Helper T cell | Third | Activated by antigen-presenting cells; activates B cells and cytotoxic T cells |
| Cytotoxic T cell | Third | Destroys infected body cells |
| Regulatory T cell | Third | Switches the immune response down |
| Memory T cell | Third | Long-lived; rapid T cell response on re-exposure |
Primary and secondary responses
The primary response to a new antigen is slow (days) and relatively small, because only a few matching lymphocytes exist at first. Because memory cells remain, the secondary response to the same antigen is faster, much larger and longer lasting, so the pathogen is usually destroyed before symptoms develop. This is the basis of immunity after infection and after vaccination.
Two exposures to the same antigen
A graph shows antibody concentration after exposure on day 0 and again on day 40. After the first exposure antibodies appear slowly, peak at a low level around day 12, then fall. After the second exposure they rise within about 2 days to a peak many times higher, and stay high for longer.
- First curve: primary response; few matching B cells, so a slow, small response.
- Second curve: secondary response; memory B cells multiply quickly into plasma cells.
- Conclusion: memory cells formed in the primary response explain long-term immunity.
Marker's note: describe the difference in speed, size and duration, then explain it with memory cells.
- Saying antibodies are cells
- Antibodies are proteins made by plasma cells.
- Describing the humoral response when asked about cell-mediated
- TASC's 2025 assessment report noted many students did this; cell-mediated means cytotoxic T cells destroying infected cells.
- Calling neutrophils antigen-presenting cells
- The antigen-presenting cells in the course are dendritic cells and macrophages.
Exam-style questions
Questions in the style of TASC exam questions on this dot point, each with a worked answer. They are written by ExamExplained unless tagged "Past paper"; the year shows the paper a question is modelled on.
Original6 marksDescribe the cell-mediated response to a virus that has infected body cells, beginning with a dendritic cell.Show worked answer →
One mark for each step, up to six.
- A dendritic cell engulfs viral particles and displays viral antigens on its surface (antigen-presenting cell).
- It presents the antigen to a helper T cell with a complementary receptor, activating it.
- The activated helper T cell divides and releases chemical signals (cytokines).
- These signals activate cytotoxic T cells with receptors complementary to the same antigen, which divide to form a clone.
- Cytotoxic T cells bind to infected body cells displaying the viral antigen and destroy them, stopping the virus replicating.
- Memory T cells remain for long-term immunity, and regulatory T cells switch the response down once the infection is controlled.
Original5 marksExplain why a person who recovered from chickenpox as a child rarely develops the disease again, referring to primary and secondary responses.Show worked answer →
- Primary response (2 marks)
- During the first infection, B and T cells with receptors specific to the chickenpox antigens were activated and multiplied; plasma cells made antibodies, and the response took days to build, so the child became ill.
- Memory cells (1 mark)
- Memory B cells and memory T cells specific to the antigen remained in the body for many years.
- Secondary response (2 marks)
- On re-exposure, memory cells recognise the antigen immediately and multiply rapidly, so antibodies are produced faster, in greater amounts and for longer. The virus is destroyed before it can cause symptoms.