Unit 12 Question Bank
The five tabs are the five sections of the real paper. Items tagged
Past Paper 2019 or 2020 are the genuine questions, reproduced verbatim.
Items tagged Slide come from the TMU lecture; items tagged Janeway's are built
from the textbook to cover examinable ground. Nothing is invented. Janeway's 10e is a reflowed
edition with no printed page numbers, so it is cited by numbered section (§1-14), not by page.
0 / 28 answered
1Which feature characterises the SECONDARY antibody response compared with the primary?
Answer: D
All five features of the secondary response move in the direction of a system that has learnt: lower threshold, shorter lag, higher rate and longer persistence, higher titre, and increased affinity and avidity. IgG predominates, not IgM. The single cause is that memory cells — numerous, already class-switched, already affinity-matured — mount the response.TMU Lecture 9 — Immune Response Slide 66 · Past Papers 2019 & 2020, Section V Q4
2Which antibody class predominates in the primary immune response?
Answer: A
IgM — the first antibody made, before class switching has occurred. IgG predominates in the secondary response because memory cells have already switched. This is also why detecting specific IgM indicates recent or current infection while IgG indicates past exposure or vaccination.TMU Lecture 9 — Immune Response Slides 64, 66 · Unit 3
3The four phases of the primary antibody response are:
Answer: B
Lag → log → plateau → decline. The lag phase is long in a primary response because a small naïve clone must first be found and then expanded; in the secondary response the lag is short because memory cells are already numerous.TMU Lecture 9 — Immune Response Slide 64
4Where do most events of the adaptive immune response take place?
Answer: C
Spleen, lymph node and MALT. The infection may be anywhere, but the response is organised where antigen is delivered and naïve lymphocytes circulate. Bone marrow and thymus are the central organs, where lymphocytes develop before ever meeting antigen.TMU Lecture 9 — Immune Response Slide 8
5In the antigen-recognition phase, how do B cells differ from T cells?
Answer: D
This asymmetry, from Unit 11, propagates through the whole response. Because the T cell reads only peptide–MHC it is MHC-restricted and sees only what an APC chooses to show; because the B cell reads native antigen it can respond to shapes and sugars the T cell never sees. Complementary sensors.TMU Lecture 9 — Immune Response Slides 9–10
6Which signals are required for full B-cell activation?
Answer: A
Signal 1 is the BCR/Igα/Igβ complex binding antigen; signal 2 is CD40 on the B cell binding CD40L on the activated Th cell. CD28–B7 is the T cell's own second signal, pointing the other way across the same synapse.TMU Lecture 9 — Immune Response Slides 56, 76
7Which cytokines from activated Th cells drive B-cell proliferation and differentiation into plasma cells?
Answer: B
These four are the cytokine half of T-cell help; the CD40–CD40L contact is the other half. A humoral response against a TD antigen needs both. IL-1/IL-12/TNF belong to innate antibacterial immunity; IL-10/TGF-β/IL-35 are suppressive.TMU Lecture 9 — Immune Response Slides 58–59
8Which is NOT one of the four effector mechanisms of antibody?
Answer: C
Antibody never kills anything by itself — it labels a target and recruits whatever does the killing. The four mechanisms are neutralisation, opsonisation and phagocytosis, ADCC, and complement activation. Only neutralisation works without recruiting anything else.TMU Lecture 9 — Immune Response Slide 60
9MHC class II restriction operates between:
Answer: D
Class II restriction: APC ↔ CD4⁺. Class I restriction: target cell ↔ CD8⁺ CTL. Remember the arithmetic — class II × CD4 = 8 and class I × CD8 = 8.TMU Lecture 9 — Immune Response Slide 74
10A TI-2 antigen activates B cells by:
Answer: A
TI-2 antigens carry many repeated determinants that cross-link the BCR and activate the mature B cell specifically. TI-1 antigens are the polyclonal activators — they carry a mitogen-like structure and at high concentration activate B cells non-specifically.TMU Lecture 9 — Immune Response Slides 69–70
11Compared with TD antigens, TI antigens produce:
Answer: B
Class switching, affinity maturation and memory all occur in the germinal centre, which requires T-cell help. A TI antigen bypasses T cells entirely, so it cannot access any of them — hence IgM only, no switch, no anamnestic response. That is why conjugating a polysaccharide to a carrier protein transforms a vaccine.TMU Lecture 9 — Immune Response Slide 72
12Why is the lag phase shorter in the secondary response?
Answer: C
One cause explains all six rows of the comparison table. Memory cells are far more numerous than the original naïve clone, so less antigen finds enough of them (threshold ↓), expansion starts sooner (lag ↓) and goes further (titre ↑); they have already switched (IgG) and already matured (affinity ↑).TMU Lecture 9 — Immune Response Slide 66 · Janeway's Immunobiology 10e
13Which cell type is responsible for mounting the secondary antibody response?
Answer: D
Memory B cells. Plasma cells from the primary response are terminally differentiated and mostly short-lived; B1 cells make only low-affinity IgM without memory. It is the memory compartment laid down during the primary response that a booster exploits.TMU Lecture 9 — Immune Response Slide 66 · Unit 8
14What is the effector phase of cell-mediated immunity?
Answer: A
Phase 3 is the effector phase. Phase 1 is antigen recognition (APC presenting to naïve T cells); phase 2 is activation, proliferation and differentiation into effector and memory cells. B-cell recognition belongs to the humoral column of phase 1.TMU Lecture 9 — Immune Response Slide 9
15Which two roles does humoral immunity play in an individual?
Answer: B
The lecture states both: humoral immunity neutralises and eliminates extracellular microbes and toxins accessible to antibody, and it mediates types I, II and III hypersensitivity. Type IV is cell-mediated, driven by Th1 — the subject of Unit 15.TMU Lecture 9 — Immune Response Slide 62
16Why does a vaccine usually require more than one dose?
Answer: C
The primary dose gives a slow, weak, low-affinity IgM response that fades — its real value is the memory compartment it establishes. The booster then produces the response that actually protects. This is the clinical face of the whole primary/secondary comparison.TMU Lecture 9 — Immune Response Slide 66 · Janeway's Immunobiology 10e
1 Immune response — 3 marks+
The process in which the immune system recognises and removes antigens. It comprises innate and adaptive responses; adaptive immunity divides into cellular immunity (primarily T-cell mediated, itself divided into CD4⁺- and CD8⁺-mediated) and humoral immunity (primarily B-cell mediated). Most events take place in the secondary (peripheral) lymphoid organs — spleen, lymph node and MALT.TMU Lecture 9 — Immune Response Slides 6–8
2 Phases of the adaptive immune response — 3 marks+
① Antigen recognition — APCs ingest, process and present antigen to naïve T cells, which recognise peptide–MHC via TCR/CD3; B cells recognise antigen directly via the BCR. ② Activation, proliferation and differentiation — naïve T cells become effector and memory T cells; naïve B cells become plasma cells and memory cells. ③ Effector — effector T cells and secreted antibodies remove the antigen.TMU Lecture 9 — Immune Response Slide 9
3 Primary antibody response — 3 marks+
The antibody response occurring on first exposure to an antigen, showing four phases: lag, log, plateau and decline. It is characterised by a high immunogen threshold, a long lag phase, a low antibody titre, predominance of IgM, and low affinity and avidity.TMU Lecture 9 — Immune Response Slide 64
4 Secondary (anamnestic) antibody response — 3 marks+
The enhanced response when a previously immunised individual is re-exposed to the same antigen, characterised by (1) a lower threshold dose of immunogen; (2) a shorter lag phase; (3) a higher rate and longer persistence of antibody synthesis; (4) a higher titre of antibody; and (5) increasing affinity and avidity — maturation of the immune response. It is mounted by memory B cells and dominated by IgG.TMU Lecture 9 — Immune Response Slide 66
5 MHC restriction in the immune response — 3 marks+
T cells recognise and respond to antigens only in association with self MHC molecules. MHC class II restriction governs the interaction between APCs and CD4⁺ T cells; MHC class I restriction governs that between target cells and CD8⁺ CTLs.TMU Lecture 9 — Immune Response Slide 74
6 TI-1 and TI-2 antigens — 3 marks+
Two subclasses of thymus-independent antigen. TI-1 antigens contain a B-cell determinant plus a mitogen-like structure, so at high concentration they act as polyclonal activators of B cells. TI-2 antigens carry many repeated determinants which cross-link the BCR and activate mature B cells specifically.TMU Lecture 9 — Immune Response Slides 69–70
1The three phases of the adaptive immune response are the ? phase, the ? , ? and ? phase, and the ? phase.5 mark(s)
The same three phases apply to both cellular and humoral immunity; only phase 1 differs between them.
TMU Lecture 9 — Immune Response Slide 92The four phases of the primary antibody response are the ? phase, ? phase, ? phase and ? phase.4 mark(s)
The lag phase is long in a primary response because a small naïve clone must first be found and expanded.
TMU Lecture 9 — Immune Response Slide 643Signal 2 for B-cell activation is the interaction between ? on the B cell and ? expressed on activated Th cells.2 mark(s)
Together with the cytokines IL-2, IL-4, IL-5 and IL-6, this is what 'T-cell help' actually consists of.
TMU Lecture 9 — Immune Response Slides 56, 764Activated Th cells secrete ? , ? , ? and ? to drive B-cell proliferation and differentiation into plasma cells.4 mark(s)
The cytokine half of T-cell help; the CD40–CD40L contact is the other half.
TMU Lecture 9 — Immune Response Slide 585The four effector mechanisms of antibody are ? , ? , ? and ? .4 mark(s)
Only neutralisation works without recruiting complement or cells — which is why F(ab′)₂ antitoxin still functions despite having no Fc.
TMU Lecture 9 — Immune Response Slide 606MHC class ? restriction operates between APCs and CD4⁺ T cells; MHC class ? restriction operates between target cells and CD8⁺ CTLs.2 mark(s)
Class II × CD4 = 8; class I × CD8 = 8.
TMU Lecture 9 — Immune Response Slide 741The secondary antibody response requires a lower threshold dose of antigen than the primary response.
TRUE
True — one of the five listed features. Memory cells are far more numerous than the original naïve clone, so much less antigen is needed to find enough of them.TMU Lecture 9 — Immune Response Slide 66
2IgG is the predominant antibody class of the primary immune response.
FALSE
False — IgM predominates in the primary response, because class switching has not yet occurred. IgG predominates in the secondary response, mounted by memory cells that have already switched.TMU Lecture 9 — Immune Response Slides 64, 66
3Thymus-independent antigens generate an anamnestic (secondary) response.
FALSE
False. TI antigens give IgM only, with no class switching and no memory cells — so there is no anamnestic response. Class switching, affinity maturation and memory all require the germinal centre, which requires T-cell help.TMU Lecture 9 — Immune Response Slide 72
4Most events of the adaptive immune response occur in the bone marrow and thymus.
FALSE
False — those are the central lymphoid organs, where lymphocytes develop before meeting antigen. Adaptive responses occur in the secondary (peripheral) organs: spleen, lymph node and MALT.TMU Lecture 9 — Immune Response Slide 8
5A humoral response against a TD antigen requires T-cell help.
TRUE
True, and the help has two components: the CD40–CD40L contact signal, and the cytokines IL-2, IL-4, IL-5 and IL-6. Without both, a B cell responding to a protein antigen cannot proliferate into plasma cells.TMU Lecture 9 — Immune Response Slide 59
6Antibody kills target cells directly.
FALSE
False. Antibody labels a target and recruits an effector — complement, a phagocyte, or an NK cell. Its four mechanisms are neutralisation, opsonisation, ADCC and complement activation, and only neutralisation works without recruiting anything.TMU Lecture 9 — Immune Response Slide 60
1
Fill in the table to compare primary and secondary humoral immune response.
6 marks
| Primary response | Secondary response | |
|---|---|---|
| Immunogen threshold | High | Low |
| Lag phase | Long | Short |
| Antibody level | Low | High, produced faster and persisting longer |
| IgM | Predominant | Present but minor |
| IgG | Little | Predominant |
| Affinity and avidity | Low | High — affinity maturation |
If there is room, give the reason in one sentence: the secondary response is mounted by memory B cells, which are already numerous, already class-switched and already affinity-matured. That single fact accounts for every row.
Marking guide: 1 mark per row. The IgM/IgG switch and the affinity row are the two that distinguish a complete answer; naming memory cells as the cause secures full marks.
2
Describe the phases of the adaptive immune response.
6 marks
| Phase | Cell-mediated immunity | Humoral immunity |
|---|---|---|
| ① Antigen recognition | APCs ingest, process and present antigen to naïve T cells, which recognise the peptide–MHC complex via TCR/CD3 | B cells recognise native antigen directly via the BCR |
| ② Activation, proliferation, differentiation | Naïve T cells are activated and differentiate into effector T cells and memory cells | Naïve B cells are activated and differentiate into plasma cells and memory cells |
| ③ Effector | Effector CD4⁺ and CD8⁺ T cells remove the antigen by various mechanisms | Antibodies secreted by plasma cells remove the antigen by neutralisation, opsonisation, ADCC and complement activation |
Add the requirements: full T-cell activation needs signal 1 + signal 2 + cytokines; full B-cell activation needs BCR signal + CD40/CD40L plus IL-2, IL-4, IL-5 and IL-6. Most events occur in the secondary lymphoid organs.
Marking guide: 1 mark per cell of the table. The phase-1 asymmetry — T cells need an APC, B cells do not — is the point most often missed.
3
Compare TD and TI antigens in the humoral immune response.
6 marks
| TD antigen | TI antigen | |
|---|---|---|
| Chemical trait | Protein | Polysaccharide |
| Th help | Needed | Not needed |
| Classes of antibody | IgG (and IgM) | IgM only |
| Class switching | + | − |
| Anamnestic response | + | − |
| Memory cells | + | − |
TI antigens subdivide: TI-1 carries a mitogen-like structure and acts as a polyclonal B-cell activator at high concentration; TI-2 carries repeated determinants that cross-link the BCR and activate mature B cells specifically.
The explanatory point worth adding: class switching, affinity maturation and memory all occur in the germinal centre, which requires T-cell help — so a TI antigen, bypassing T cells, can access none of them.
Marking guide: 1 mark per row. Distinguishing TI-1 from TI-2, or explaining why no T help means no memory, earns the final marks.