The shape of the lesson
By the end of the lesson, learners can
- The primary response: Press Next step to work through all eight steps.
- Memory and the secondary response: Press First infection and watch the graph, then press Same pathogen again.
- Macrophage presents; T-helper selected, cloned, releases cytokines.
- B cell selected and cloned; becomes plasma cells + memory cells.
- T-killer cells destroy infected body cells.
- Secondary response: sooner, larger, longer, thanks to memory cells.
One picture every idea returns to
In a primary immune response a macrophage engulfs a pathogen and presents its antigens. The one T-helper cell with complementary receptors binds (clonal selection) and divides by mitosis (clonal expansion); its clones release cytokines. The B-lymphocyte with complementary receptors, stimulated by cytokines, divides into a clone that differentiates into plasma cells, which secrete specific antibodies, and memory cells. Cytokines also activate T-killer cells, which destroy infected body cells displaying the antigen. Because selection and cloning take days, the primary response is slow. Memory cells stay in the blood for years, so a second exposure to the same antigen triggers a secondary response that is faster and much larger: this is long-term immunity.
Forty-five minutes, phase by phase
| Time | Phase | What happens in the room | Grouping |
|---|---|---|---|
| 0 to 5 min | Hook: predict | Open with the question in the title, Pick the right cell, then copy it.. Your blood holds millions of different lymphocytes, each with receptors of one shape. Put the figure on the board: it is the one picture every idea in the lesson returns to. | Whole class, then pairs |
| 5 to 17 min | Teach and check: The primary response | Press Next step to work through all eight steps. Project tab 3 of the lab (Immunity lab, primary immune response) and let a student drive it while the class predicts. | Whole class, then pairs |
| 17 to 30 min | Teach and check: Memory and the secondary response | Press First infection and watch the graph, then press Same pathogen again. Project tab 4 of the lab (Immunity lab, memory cells and the secondary response) and let a student drive it while the class predicts. | Think-Pair-Share |
| 30 to 36 min | Check | The four Stage 1 questions from the student lesson, answered on mini whiteboards or by show of fingers. Re-teach the one most get wrong. | Individual, then whole class |
| 36 to 43 min | Plenary | The exam-style questions from Stage 2, one at a time: thirty seconds alone, then a random call. The feedback lines in the key give the examiner's wording. | Individual, random call |
| 43 to 45 min | Exit and homework | Set the worksheet below (6 questions, 20 marks). Learners self-assess against the objectives before they leave. | Individual |
Protect the parts that carry the learning
The sequence carries about fifty minutes of material, so the lab is driven by one student while the class predicts rather than explored freely. Times are a guide.
Protected: the check at 30 minutes. It is the only individual read on whether the key idea landed, and it is not cut.
Cut first if the build overruns: the last check in Memory and the secondary response, never the check or the plenary.
In a 60 minute block: run worksheet questions 1 to 3 in class as a Rally Coach set and model both the hardest worked example and its check live.
Think-Pair-Share
Pose the question, give thirty seconds of silent thinking, then a minute to compare with a partner before a few pairs share with the class. The silent minute is the part that cannot be cut.
The full structure, with its variations and the other twelve, is on the cooperative-learning page.
What to head off, and how
| Trap learners fall into | Teaching move that pre-empts it |
|---|---|
| Clonal selection is not the lymphocyte "making" a receptor to fit the antigen. | The lymphocyte with a complementary receptor already exists before the infection; the antigen only selects it. |
| Long-term immunity is due to memory cells, not to antibodies staying in the blood. | Antibodies are broken down within weeks; memory cells remain. |
Lymphocytes and the immune response: worksheet
6 questions, 20 marks. Written in the style of the papers; no past paper question is reproduced.
Describe the sequence of events in a primary immune response to a bacterium, from the bacterium entering the blood to the secretion of antibodies.
Plasma cells contain large amounts of rough endoplasmic reticulum, many Golgi bodies and many mitochondria. Explain how these features relate to their function.
A person's blood was tested after two exposures to the same antigen, 40 days apart. After the first exposure, antibody was first detected on day 7 and peaked at 10 arbitrary units on day 14. After the second exposure, antibody was detected within 2 days and peaked at 100 arbitrary units on day 46. Describe and explain the differences between the two responses.
Explain why a person with an infection usually feels ill for several days before they start to recover during a primary immune response.
Compare the roles of T-helper cells and T-killer cells.
Explain the role of memory cells in long-term immunity.
Answer key and marking notes
- A macrophage engulfs the bacterium and presents its antigens on its cell surface membrane.
- A T-helper cell with complementary receptors binds to the presented antigen (clonal selection).
- The T-helper cell divides by mitosis (clonal expansion) and releases cytokines.
- A B-lymphocyte with complementary receptors binds the antigen and, stimulated by cytokines, divides by mitosis into a clone.
- The clone differentiates into plasma cells, which secrete specific antibodies, and memory cells.
- Antibodies are proteins, made by ribosomes on the rough ER.
- The Golgi body modifies and packages the antibodies into vesicles for exocytosis.
- Mitochondria supply ATP for protein synthesis and for the secretion of large amounts of antibody.
- Second response starts sooner (2 days compared with 7 days).
- Second response peaks ten times higher (100 compared with 10 units) and antibody stays high for longer.
- Memory B cells made in the first response are present in much larger numbers than the original matching lymphocytes.
- So clonal selection is immediate and memory cells divide rapidly into many plasma cells.
- Only a few lymphocytes have receptors complementary to the new antigen.
- Clonal selection, clonal expansion and differentiation into plasma cells take several days.
- During this time the pathogen multiplies and damages tissues, causing symptoms.
- Both are T-lymphocytes with specific receptors that are selected and cloned in response to an antigen.
- T-helper cells release cytokines that stimulate B cells to divide and form plasma cells, and activate T-killer cells and macrophages.
- T-killer cells bind to and destroy infected body cells displaying the antigen; they do not stimulate B cells.
- Memory cells are long-lived and remain in the blood for years after the infection.
- On re-infection with the same antigen they give a rapid secondary response, so the pathogen is destroyed before it causes disease.
8 multiple-choice questions on this lesson
From the topic question bank. Assign them in the app for a marked score in your gradebook, or run the topic as a class game.
Where do B-lymphocytes and T-lymphocytes mature?
- AB cells in the bone marrow; T cells in the thymus
- BB cells in the thymus; T cells in the bone marrow
- Cboth in the lymph nodes
- Dboth in the spleen
What is the main role of the cytokines released by activated T-helper cells?
- Ato stimulate the selected B cells to divide and differentiate, and to activate T-killer cells
- Bto bind to antigens on the pathogen and cause agglutination
- Cto make holes in the membranes of infected body cells
- Dto present antigens on the surface of macrophages
Which sequence describes the primary immune response in the correct order?
- Aantigen presentation, clonal selection, clonal expansion, differentiation into plasma cells
- Bclonal expansion, antigen presentation, clonal selection, differentiation into plasma cells
- Cclonal selection, differentiation into plasma cells, antigen presentation, clonal expansion
- Ddifferentiation into plasma cells, clonal selection, clonal expansion, antigen presentation
The graph shows the antibody concentration in a person's blood after injection of an antigen at time X and again at time Y. What is the main reason for the difference between the two peaks?
- Amemory cells formed after X divide rapidly into plasma cells after Y
- Bantibodies made after X are still circulating at Y
- Cthe second dose of antigen was much larger than the first
- Dphagocytes remember the antigen after the first injection
Which feature is typical of a plasma cell?
- Aextensive rough endoplasmic reticulum
- Ba lobed nucleus and many lysosomes
- Creceptors that bind to infected body cells
- Dchloroplasts and a large vacuole
Use the graph. What is the ratio of the peak antibody concentration after Y to the peak after X?
- Aabout 12 : 1
- Babout 1 : 12
- Cabout 3 : 1
- Dabout 120 : 1
A drug used after organ transplants stops T-helper cells from releasing cytokines. Which effect on the patient's immune system is expected?
- Afewer plasma cells and fewer activated T-killer cells form in response to the transplant's antigens
- Bmacrophages can no longer engulf pathogens
- Cthe transplanted organ's cells lose their non-self antigens
- Dexisting antibodies in the blood are broken down immediately
Mice were exposed to antigen A on day 0. On day 30, half the mice were exposed to antigen A again and half were exposed to a new antigen B. Which result would you expect in the following week?
- Aa fast, large response to A, but a slow, small primary response to B
- Ba fast, large response to both A and B
- Ca slow, small response to both A and B
- Da fast, large response to B, but a slow, small response to A
Quiz key
Both types are made from stem cells in the bone marrow; B cells mature there, while T cells move to the thymus to mature. Swapping the two organs is the common error. Lymph nodes and the spleen are where mature lymphocytes meet antigens and are activated, not where they mature.
Cytokines are cell-signalling molecules: they stimulate B-lymphocytes to undergo clonal expansion and form plasma cells, and they activate T-killer cells and macrophages. Agglutination is caused by antibodies. Making holes in infected cells is done by T-killer cells. Antigen presentation is done by macrophages themselves, using antigens from a digested pathogen.
The antigen is presented first; the lymphocyte with a complementary receptor is then selected; it divides by mitosis to form a clone; and the clone differentiates into plasma cells (and memory cells). Any order that puts expansion before selection, or plasma cells before division, cannot work, because the right cell must be chosen before it is copied.
By the time of Y the antibody level has returned to almost zero, so antibodies from X are not the reason. Memory B cells, formed after X, are present in large numbers, recognise the antigen at once and divide rapidly into plasma cells, giving a faster, larger response. Nothing suggests a larger dose, and dose alone would not explain the much shorter delay. Phagocytes are non-specific and do not form memory.
Plasma cells secrete antibodies, which are proteins, so they have large amounts of rough ER (and Golgi and mitochondria). A lobed nucleus and many lysosomes describe a neutrophil. Binding infected body cells is the job of T-killer cells. Chloroplasts and a large vacuole belong to plant cells.
The first peak is about 10 units and the second about 116 units, so the ratio is about 12 : 1. 1 : 12 reverses the order asked for. 3 : 1 compares the second peak with the 40-unit gridline rather than the first peak. 120 : 1 uses the top of the axis and a peak of 1, misreading both values.
Without cytokines, selected B cells are not stimulated to divide into plasma cells and T-killer cells are not activated, so the transplant is less likely to be rejected (but infections become more likely). Macrophages can still carry out phagocytosis, although less actively. The donor's antigens are unchanged; the drug acts on the recipient's cells. The drug does not destroy antibodies already present; they are broken down at their normal rate.
Memory cells made after day 0 have receptors complementary to antigen A only, so A gives a secondary response, while B meets only the few naive lymphocytes that match it and gives a primary response. A fast response to B would need memory cells for B, which do not exist. A slow response to A ignores the memory cells. Reversing the two responses confuses which antigen was met first.
What to project
The student lesson embeds these tabs. Open them full screen on the projector; every slider has a drag handle on the stage.
Slides for this lesson
A projectable deck for every pack is on the way. Until then, present the student lesson full screen: its sections, figure and lab tabs follow the same order as the plan above.