Unit 7 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 / 30 answered
1Which of the following cells participates in adaptive immunity?
Answer: B
αβ T cells. They alone have enormous TCR diversity and are MHC-restricted — the hallmarks of clonal selection. γδ T cells have limited diversity, are not MHC-restricted and sit in skin and mucosa; B1 cells make IgM without T help or class switching; NKT cells have a near-invariant receptor. All three are innate-like lymphocytes.Past Papers 2019 & 2020, Section III Q11 — verbatim, both years
2Which of the following molecules is expressed on T cells?
Answer: C
CD40L (CD154), on activated T cells; its ligand is CD40 on B cells and APCs. The three distractors — CD19, CD21 and CD81 — are precisely the three components of the B-cell co-receptor complex. Remember the pairing: CD40L on the T cell, CD40 on the B cell.Past Papers 2019 & 2020, Section III Q13 — verbatim, both years
3Among the following molecules, which one can down-regulate T cell activation?
Answer: D
CTLA-4 (CD152). It binds the same ligands as CD28 — B7.1 and B7.2 — but with higher affinity, and it carries an ITIM instead of an activating motif, so it delivers an inhibitory signal. It is induced only after activation, making it a built-in off-switch. CD28 is the accelerator; CD3 signals for the TCR; CD2 is adhesion and co-stimulation.Past Papers 2019 & 2020, Section III Q16 — verbatim, both years
4Positive selection of thymocytes occurs where, and confers what?
Answer: A
Positive selection happens in the cortex at the double-positive stage, presented by thymic epithelial cells. Cells recognising self-peptide–MHC with proper affinity survive; those that cannot recognise it at all are useless and die. The result is MHC restriction. Negative selection, in the medulla at SP stage, is what confers tolerance.TMU Lecture 7 — Immune Cells Slide 90
5During negative selection, a thymocyte dies if it:
Answer: B
High-affinity recognition of self means the cell is potentially autoreactive, so it is deleted by apoptosis — this is how self-tolerance is established. Note the inversion: failing to recognise is fatal during positive selection but survivable during negative selection.TMU Lecture 7 — Immune Cells Slide 91
6Which cells present self-peptide–MHC during negative selection?
Answer: C
Dendritic cells and macrophages, at the cortico-medullary junction and in the medulla. Thymic epithelial cells are the presenters during positive selection in the cortex — different cell, different location, opposite outcome.TMU Lecture 7 — Immune Cells Slides 90–91
7In the TCR–CD3 complex, the role of CD3 is:
Answer: D
The TCR binds antigen but has almost no cytoplasmic tail, so it cannot signal. CD3 supplies that, through ITAM motifs in its cytoplasmic tails. Both are lineage-specific markers of T cells. The same division of labour reappears in the BCR, where Igα/Igβ do CD3's job.TMU Lecture 7 — Immune Cells Slides 102–103
8ITAM motifs are characterised by:
Answer: A
Immunoreceptor tyrosine-based activation motif. The mirror image is ITIM — the same architecture used for inhibition, found in CTLA-4 and PD-1. Activation and inhibition are built from the same part.TMU Lecture 7 — Immune Cells Slide 102
9MHC restriction means that:
Answer: B
A given T cell sees peptide only in the context of self-MHC. It is acquired during positive selection, so the MHC haplotype of the thymus in which a T cell develops determines its restriction for life. CD8⁺ CTLs are class-I restricted; CD4⁺ helpers are class-II restricted.TMU Lecture 7 — Immune Cells Slides 98, 100
10CD4 acts as a co-receptor by binding which part of the MHC molecule?
Answer: C
The β2 domain of MHC class II — a non-polymorphic region away from the peptide groove, so the grip is the same whatever peptide is displayed. CD8 correspondingly binds the α3 domain of MHC class I.TMU Lecture 7 — Immune Cells Slides 105, 107
11CD4 is the cellular receptor for which viral protein?
Answer: D
HIV gp120. This single fact shapes the whole disease: the virus enters through the molecule that defines the helper T cell, depleting exactly the population that coordinates both arms of adaptive immunity. EBV uses CD21 — the B-cell complement receptor from Unit 6.TMU Lecture 7 — Immune Cells Slides 105–106
12The second (co-stimulatory) signal for T-cell activation is delivered by:
Answer: A
CD28 with B7.1 (CD80) / B7.2 (CD86) on the APC. TCR–CD3 with peptide–MHC is signal 1; local cytokines are signal 3, directing which effector type the cell becomes. B7 appears on an APC only after it has met a pathogen — so signal 2 is effectively innate immunity vouching for the threat.TMU Lecture 7 — Immune Cells Slides 109, 112
13A T cell that receives signal 1 without signal 2 will:
Answer: B
Anergy — functional inactivation. This is peripheral tolerance, a second safety net catching self-reactive cells that escaped thymic negative selection. Recognising something is deliberately not sufficient reason to attack it.TMU Lecture 7 — Immune Cells Slides 108–109 · Janeway's Immunobiology 10e
14Which pair correctly matches a co-inhibitory receptor with its ligand?
Answer: C
PD-1 binds PD-L1 and PD-L2. CD28 binds B7.1/B7.2, not CD40; ICOS binds ICOSL (B7-H2); CD2 binds LFA-3 (CD58). Tumours frequently over-express PD-L1 to switch off infiltrating T cells, which is what checkpoint inhibitors block.TMU Lecture 7 — Immune Cells Slides 117, 128
15Regulatory T cells are characterised by which combination?
Answer: D
CD4⁺CD25⁺, with FoxP3 as the master transcriptional regulator — its expression is necessary and sufficient to induce the Treg lineage. Tregs maintain tolerance to self and prevent autoimmune disease, suppressing via IL-10 and TGF-β and by killing activated T cells directly.TMU Lecture 7 — Immune Cells Slides 147–148
16Which cytokines are produced by Th17 cells?
Answer: A
IL-17, IL-17F and IL-22 (also IL-21). Because IL-17 and IL-22 receptors are so widely distributed, Th17 responses produce a massive tissue reaction — good against extracellular bacteria and fungi, but a contributor to several inflammatory diseases. IL-10 and TGF-β are the Treg suppressive cytokines.TMU Lecture 7 — Immune Cells Slide 150
1 MHC restriction — 3 marks+
The fact that a given T cell will recognise a peptide antigen only when it is bound to a particular MHC molecule — normally self-MHC. It is acquired during positive selection, so the MHC haplotype of the thymus in which a T cell develops determines its restriction. Recognition by CD8⁺ CTLs is restricted by MHC class I; responses of CD4⁺ helper T cells are restricted by MHC class II.TMU Lecture 7 — Immune Cells Slides 98, 100
2 Positive selection — 3 marks+
Selection occurring in the thymic cortex at the double-positive stage, in which DP thymocytes interact with thymic epithelial cells bearing self-peptide–MHC complexes. Cells recognising with proper affinity survive; those unable to recognise, or recognising with high affinity, die by apoptosis. Result: self-MHC restriction, and commitment to CD4 (class II) or CD8 (class I).TMU Lecture 7 — Immune Cells Slide 90
3 Negative selection — 3 marks+
Selection occurring at the cortico-medullary junction and thymic medulla at the single-positive stage, in which SP cells interact with thymic dendritic cells and macrophages. Cells recognising self-peptide–MHC with high affinity undergo apoptosis; those recognising weakly or not at all survive and mature. Result: self-immune tolerance.TMU Lecture 7 — Immune Cells Slide 91
4 TCR–CD3 complex — 3 marks+
The T-cell antigen receptor together with CD3. TCR performs antigen binding and is a lineage-specific marker; CD3 performs signal transduction from the TCR and is also lineage-specific. CD3's cytoplasmic tails carry ITAM motifs — two tyrosines about 10 residues apart, phosphorylated on activation. TCRs are αβ (95–99%) or γδ (1–5%).TMU Lecture 7 — Immune Cells Slides 95, 102–103
5 Double signals for T-cell activation — 3 marks+
Signal 1 — the TCR signal: the TCR–CD3 complex recognises the antigen–MHC complex, with CD4 or CD8 as co-receptor. Signal 2 — the co-stimulatory signal: CD28 on the T cell binds B7.1 (CD80) / B7.2 (CD86) on the APC. A third set of signals, from local cytokines, directs differentiation into distinct effector types. Signal 1 without signal 2 causes anergy.TMU Lecture 7 — Immune Cells Slides 108–110
6 CTLA-4 (CD152) — 3 marks+
A T-cell surface molecule induced on activation and absent from resting cells. It binds B7.1 and B7.2 — the same ligands as CD28 — but carries an ITIM (immunoreceptor tyrosine-based inhibition motif) and therefore delivers inhibitory signals. It is an important negative regulator of T-cell activation and is critical for maintaining T-cell homeostasis.TMU Lecture 7 — Immune Cells Slide 114
7 Regulatory T cells (Treg) — 3 marks+
A subpopulation of T cells that modulate the immune system, maintain tolerance to self-antigens and prevent autoimmune disease. They express CD4 and CD25, with FoxP3 as the master transcriptional regulator — necessary and sufficient to induce the lineage. They suppress by secreting IL-10 and TGF-β and by killing activated T cells directly. Thymic Treg develop in the thymus; peripheral Treg differentiate in the periphery.TMU Lecture 7 — Immune Cells Slides 147–148
8 Cytotoxic T lymphocyte (CTL) — 3 marks+
A CD8⁺ effector T cell whose function is to directly kill target cells. Its characteristics are antigen specificity, MHC class I restriction, and that the CTL is not injured while killing. Two mechanisms: the perforin/granzyme pathway and the Fas–FasL pathway, both ending in caspase activation and apoptosis.TMU Lecture 7 — Immune Cells Slides 154–157
1T cells develop in the thymus through three stages: ? , ? and ? .3 mark(s)
DN is CD4⁻CD8⁻, DP is CD4⁺CD8⁺, SP is CD4⁺CD8⁻ or CD4⁻CD8⁺.
TMU Lecture 7 — Immune Cells Slides 86–872Positive selection occurs in the thymic ? and confers ? ; negative selection occurs in the ? and confers ? .4 mark(s)
Both show the cell self-peptide–MHC, but they want opposite affinities: proper affinity passes positive selection, high affinity fails negative selection.
TMU Lecture 7 — Immune Cells Slides 90–913In the TCR–CD3 complex, ? binds antigen and ? transduces the signal via ? motifs.3 mark(s)
The same architecture recurs in the BCR, where Igα/Igβ carry the ITAMs.
TMU Lecture 7 — Immune Cells Slides 102–1034CD4 binds the ? domain of MHC class ? ; CD8 binds the ? domain of MHC class ? .4 mark(s)
Both bind non-polymorphic regions away from the peptide groove, so the grip does not depend on which peptide is displayed.
TMU Lecture 7 — Immune Cells Slides 105, 1075The first signal for T-cell activation is delivered by the ? complex recognising ? ; the second signal is delivered by ? binding ? .4 mark(s)
Signal 1 says “I found my antigen”; signal 2 says “and it is genuinely dangerous”, because B7 appears only on APCs that have met a pathogen.
TMU Lecture 7 — Immune Cells Slide 1096Positive co-stimulatory molecules include ? and ? ; negative (coinhibitory) molecules include ? and ? .4 mark(s)
The deck's own metaphor: accelerator and brake. Together they are the immune checkpoints, and blocking the brakes is the basis of checkpoint-inhibitor cancer therapy.
TMU Lecture 7 — Immune Cells Slide 1187CTLs kill target cells by two mechanisms: the ? / ? pathway and the ? – ? pathway.4 mark(s)
Perforin polymerises to form an aqueous channel; granzymes enter through it and activate caspases. FasL on the CTL binds Fas on the target. Both end in apoptosis.
TMU Lecture 7 — Immune Cells Slides 156–1578Regulatory T cells express ? and ? on the surface, with ? as the master transcriptional regulator, and suppress using ? and ? .5 mark(s)
FoxP3 expression is necessary and sufficient to induce the Treg lineage; losing it causes IPEX syndrome, overwhelming multi-organ autoimmunity from birth.
TMU Lecture 7 — Immune Cells Slides 147–1481Effector CTLs specifically kill target cell by releasing perforin, granzyme and expressing FasL.
TRUE
TRUE. Both mechanisms are named correctly, and so are the verbs: perforin and granzyme are released from granules, while FasL is expressed on the CTL surface. A statement saying the CTL releases FasL would be false.Past Papers 2019 & 2020, Section IV Q5 — verbatim, both years
2A mature αβ T cell can express both CD4 and CD8 simultaneously.
FALSE
False. Co-expression happens only transiently at the double-positive stage inside the thymus. Positive selection then commits the cell to one or the other, according to whether its TCR engaged MHC class I (→CD8) or class II (→CD4).TMU Lecture 7 — Immune Cells Slides 87, 104
3CTLA-4 and CD28 bind the same ligands.
TRUE
True — both bind B7.1 (CD80) and B7.2 (CD86). The difference is the signal delivered: CD28 activates, while CTLA-4 binds with higher affinity and carries an ITIM, delivering inhibition. That shared ligand is exactly what makes MCQ Q16 a good question.TMU Lecture 7 — Immune Cells Slide 114
4γδ T cells recognise antigen in an MHC-restricted manner.
FALSE
False. γδ T cells are not MHC-restricted, have limited TCR diversity, and sit in skin and mucosal tissue. They are classed as innate immune cells — which is why MCQ Q11's answer is αβ, not γδ.TMU Lecture 7 — Immune Cells Slide 134
5A T cell receiving only signal 1 becomes fully activated.
FALSE
False — it becomes anergic. The lecture states plainly that a T cell cannot be activated with a single signal. This requirement is a deliberate safety feature: recognising an antigen is not sufficient reason to attack it.TMU Lecture 7 — Immune Cells Slides 108–109
6During positive selection, thymocytes that cannot recognise self-peptide–MHC survive.
FALSE
False. In positive selection, failure to recognise is fatal — such a cell could never see antigen on your own MHC and is useless, so it dies by apoptosis. It is during negative selection that weak or absent recognition is what lets a cell survive.TMU Lecture 7 — Immune Cells Slides 90–91
1
Compare positive and negative selection of T lymphocytes.
6 marks
| Positive selection | Negative selection | |
|---|---|---|
| Location | Thymic cortex | Cortico-medullary junction and medulla |
| Stage | Double-positive (DP) | Single-positive (SP) |
| Presented by | Thymic epithelial cells | Thymic dendritic cells and macrophages |
| Survive | Recognise self-peptide–MHC with proper affinity | Cannot recognise, or recognise with low affinity |
| Die | Cannot recognise, or recognise with high affinity | Recognise with high affinity |
| Result | Self-MHC restriction; commitment to CD4 or CD8 | Self-immune tolerance |
Marking guide: 1 mark per row. The result row carries most weight — an answer that does not state restriction vs tolerance cannot reach full marks.
2
Describe the surface molecules of T lymphocytes and their functions.
6 marks
① TCR–CD3 complex. TCR binds antigen (αβ 95–99%, γδ 1–5%) and is a lineage marker; CD3 transduces the signal through ITAM motifs.
② Co-receptors. CD4 (monomer, 60–65% of αβ T cells) binds the β2 domain of MHC class II and is the HIV gp120 receptor; CD8 (heterodimer, 30–35%) binds the α3 domain of MHC class I. Both increase antigen sensitivity and participate in activation signalling.
③ Co-stimulatory molecules. Positive: CD28 (ligand B7.1/B7.2 — signal 2), ICOS (ligand ICOSL). Negative: CTLA-4 (same B7 ligands, ITIM, inhibitory), PD-1 (ligands PD-L1/PD-L2). Also CD40L (ligand CD40 on B cells/APC), CD2 (ligand LFA-3), LFA-1 (ligand ICAM-1).
④ Mitogen receptors. PHA, Con A, PWM — polyclonal, non-specific activators used in the T-cell transformation test.
Marking guide: 1.5 marks per group. Naming ligands as well as molecules is what separates full marks; the CD28/CTLA-4 contrast is the highest-value single point.
3
How do cytotoxic T lymphocytes kill their target cells?
6 marks
Characteristics. CTLs are CD8⁺, kill with antigen specificity and MHC class I restriction, and are not injured in the process — so one CTL can kill repeatedly.
① Perforin / granzyme pathway. Perforin, a pore-forming monomer stored in CTL granules, is released and polymerises to form an aqueous channel in the target membrane; the target may die by osmotic swelling. Granzymes enter through these channels, activate caspases and induce apoptosis.
② Fas–FasL pathway. The CTL expresses FasL, which binds Fas on the target cell; this activates caspases and causes apoptosis.
Both pathways converge on apoptosis rather than lysis — which destroys the viral genome and packages the remains for phagocytosis instead of spilling infectious virions into the tissue.
Marking guide: 2 marks for the characteristics, 2 for each pathway. Naming perforin's pore-forming action and granzyme's caspase activation separately is expected.