BIOLOGY WITH HAMZA · MDCAT REVISION
Immunity
Name: ____________________ Date: ______________
Recall first. Check second. Return to the ideas you missed.
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Learning targets
- Compare innate and adaptive immune responses.
- Explain clonal selection of B and T lymphocytes.
- Distinguish active from passive immunity and primary from secondary responses.
Core notes
- Innate defences are rapid and pattern-based.
- Adaptive responses depend on antigen-specific clonal selection.
- B cells support antibody-mediated defence; T cells coordinate and kill infected cells.
- Memory cells make later responses faster and stronger.
Read, cover and redraw
Pathogen or damage signals are detected.
Blood flow and permeability increase.
Innate cells engulf and process material.
Specific T cells are activated.
Effector and memory cells expand.
Written recall
1. Why does passive immunity not usually produce long-term immune memory?
2. How can a phagocyte help start an adaptive response?
3. What is clonal selection?
4. Why can the later response start faster?
5. Are antibodies sufficient for every infected cell?
Apply the idea
1. Which explanation best fits the response pattern?
| Exposure | Days to detectable antibody | Peak relative level |
|---|---|---|
| First | 7 | 20 |
| Second | 2 | 120 |
- Antigen-specific memory produced by the first exposure
- The second dose contains no antigen
- Innate skin barriers alone manufacture antibodies
- Every antibody molecule divides into two
My answer: _____ Reason: ____________________________________
2. A person receives ready-made antibodies. Which feature distinguishes this protection from vaccination-induced active immunity?
- A delayed response requiring weeks before any antibody is present
- Immediate protection without the recipient generating those antibodies or memory from the transfer itself
- Permanent protection guaranteed after one dose
- Transfer of a complete new immune system
My answer: _____ Reason: ____________________________________
3. Why does an antibiotic that blocks bacterial cell-wall synthesis fail to target influenza replication directly?
- Influenza replicates without a genome
- All viruses have thicker peptidoglycan walls
- Influenza does not build a bacterial peptidoglycan wall
- Antibiotics cannot enter any human tissue
My answer: _____ Reason: ____________________________________
Answer key
Cover this section while attempting the questions.
Written recall
1. The recipient receives antibodies rather than activating and cloning their own antigen-specific lymphocytes.
2. It processes engulfed material and presents antigen fragments that contribute to activation of specific T lymphocytes.
3. Activation and expansion of lymphocytes with receptors matching an antigen.
4. Antigen-specific memory populations already exist.
5. No. Cell-mediated mechanisms also contribute.
Applied questions
1. A — A faster, stronger response to the same antigen is consistent with memory lymphocytes formed during the first adaptive response.
2. B — Transferred antibodies can act quickly but are eventually broken down. The transfer itself does not create antigen-specific memory in the recipient.
3. C — The drug’s target is a bacterial structure absent from influenza. A therapy needs a relevant target; this does not imply antibiotics never have a role in a separate bacterial coinfection.