Unit 8 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 / 29 answered
1Which molecule on B cells delivers the most important second signal of B cell activation?
Answer: D
CD40. Read the question carefully — it asks for the molecule on B cells. CD40L is on the activated T cell, so it is the ligand, not the answer. CD28 is the T cell's own second-signal receptor. The BCR delivers signal one. Every distractor is a real molecule from the same story, placed on the wrong cell or at the wrong step.Past Papers 2019 & 2020, Section III Q10 — verbatim, both years
2Which of the following molecules is expressed on B cells?
Answer: A
CD20, the B-cell-specific marker and the target of rituximab. CD2 and CD3 are T-cell molecules; PD-1 is the inhibitory receptor mainly on activated T cells. Note that CD20 is the correct answer here as a B-cell marker but the wrong answer in True/False Q2 as a co-receptor component — both questions test whether you know what it actually does.Past Papers 2019 & 2020, Section III Q12 — verbatim, both years
3The B-cell co-receptor complex consists of:
Answer: B
CD19, CD21, CD81. Substituting CD20 for CD21 is exactly the trap in True/False Q2 — a single-digit change that turns a true statement false. CD21 is CR2, the C3d receptor, which is why complement-tagged antigen lowers the B cell's activation threshold — and why EBV, which uses CD21, infects B cells.TMU Lecture 7 — Immune Cells Slide 180
4Which surface immunoglobulins mark a mature naïve B cell?
Answer: C
mIgM and mIgD together. The whole developmental sequence is legible from surface Ig: pro-B has none, pre-B has the pre-BCR, immature B has mIgM alone, mature B has mIgM + mIgD, and the plasma cell has none at all because it now secretes antibody instead.Past Papers 2019 & 2020, Section IV Q6 · TMU Lecture 7 — Immune Cells Slides 167, 179
5In the BCR complex, signal transduction is performed by:
Answer: D
Igα/Igβ, through ITAM motifs — exactly the role CD3 plays for the TCR. Membrane Ig binds antigen but cannot signal. One design, two receptors: if you can state it for the T cell you can state it for the B cell.TMU Lecture 7 — Immune Cells Slide 178
6Which is NOT a mechanism of central tolerance in B cells?
Answer: A
B cells use clonal deletion, receptor editing and anergy. Positive selection is a T-cell process — it establishes MHC restriction, which B cells do not need because the BCR reads native antigen directly rather than peptide on MHC.TMU Lecture 7 — Immune Cells Slide 168
7Receptor editing in B-cell development refers to:
Answer: B
A self-reactive immature B cell gets a second attempt at its own receptor by re-rearranging the light-chain gene. It is the only place in immunology where a lymphocyte can revise its specificity rather than being deleted — worth it because the cell is usually self-reactive through one unlucky chain, not because the whole cell is wrong.TMU Lecture 7 — Immune Cells Slide 170
8CD21 on B cells is the receptor for:
Answer: C
C3d (as CR2) and EBV. The complement link matters: an antigen already tagged with C3d engages both the BCR and the co-receptor at once, sharply lowering the activation threshold — innate immunity vouching for the antigen. EBV exploits the same receptor to enter B cells.TMU Lecture 7 — Immune Cells Slide 180
9Which molecule negatively regulates the B-cell co-receptor via an ITIM motif?
Answer: D
CD22 carries an ITIM in its cytoplasmic tail and dampens CD19/CD21/CD81 signalling. CD32 is the other negative regulator, restraining activation and antibody secretion. Note the recurring pattern: ITAM activates, ITIM inhibits.TMU Lecture 7 — Immune Cells Slide 188
10B7-1 (CD80) and B7-2 (CD86) on a B cell serve to:
Answer: A
They point outward. B7 on the B cell engages CD28 on the T cell, giving the T cell its signal 2 — while the T cell's CD40L gives the B cell its signal 2 through CD40. Each cell supplies the other's licence, which is the whole mechanism behind T-dependent antigens.TMU Lecture 7 — Immune Cells Slide 186
11Which is a characteristic of B1 cells?
Answer: B
B1 cells are innate lymphocytes: derived from fetal liver, self-renewing, sitting in the peritoneal and pleural cavities and intestinal lamina propria, responding to TI antigens with low-affinity multi-reactive IgM — no T help, no class switching, no memory. The other three options describe B2 cells.TMU Lecture 7 — Immune Cells Slides 194–196
12Plasma cells are characterised by:
Answer: C
A plasma cell has no surface Ig — it secretes it instead — and does not divide. Some migrate to bone marrow and survive for years; others die within one or two weeks. The secreted antibody has the identical specificity to the BCR the cell started with.TMU Lecture 7 — Immune Cells Slides 174, 193
13Why are B cells especially important for presenting soluble antigen?
Answer: D
A macrophage takes up whatever floats past; a B cell uses its antigen-specific receptor as the collecting tool, concentrating its own antigen enormously before presenting it on MHC class II. At low antigen concentrations that is a decisive advantage — and the B cell is rewarded with CD40L help from the very T cell it activates.TMU Lecture 7 — Immune Cells Slide 209
14Regulatory B cells (Breg) suppress immune responses by secreting:
Answer: A
IL-10, TGF-β and IL-35, and they also express FasL and PD-L1 to engage Fas and PD-1 on targets. Note the overlap with Treg cells, which also use IL-10 and TGF-β — suppression has a shared vocabulary. IL-2/IFN-γ/TNF is Th1, IL-4/IL-5/IL-13 is Th2, IL-17/IL-22 is Th17.TMU Lecture 7 — Immune Cells Slide 210
15Which antibody functions are mediated through the Fc receptor?
Answer: B
All three are Fc-dependent, as Unit 3 established. Neutralisation, by contrast, needs only the variable region — which is why pepsin-digested F(ab′)₂ antitoxin still works. Complement activation is Fc-dependent but is a separate route from Fc-receptor binding.TMU Lecture 7 — Immune Cells Slide 200
16CD19 is clinically important primarily as:
Answer: C
CD19 is the CAR-T target; CD20 is the rituximab target; CD21 is the EBV receptor; CD40 is the second-signal receptor. All four distractors are true statements about different molecules — which is precisely the discrimination this unit's four exam items test.TMU Lecture 7 — Immune Cells Slide 188 · Janeway's Immunobiology 10e
1 BCR complex — 3 marks+
The B-cell antigen receptor complex. BCR is membrane-associated immunoglobulin (mIg), which binds specific antigen through VH + VL. Igα (CD79a) and Igβ (CD79b) associate with mIg and perform signal transduction into the B cell through ITAM motifs — the same role CD3 plays for the TCR.TMU Lecture 7 — Immune Cells Slide 178
2 B-cell co-receptor — 3 marks+
A complex of CD19, CD21 and CD81 which enhances the ability of naïve B cells to respond to antigen and transduces the first signal together with Igα/Igβ. CD21 is CR2, the receptor for complement C3d and for Epstein–Barr virus. CD20 is NOT part of this complex.TMU Lecture 7 — Immune Cells Slide 180
3 Double signals for B-cell activation — 3 marks+
Signal 1 — the BCR signal: the BCR complex binds antigen, with CD19/CD21/CD81 as co-receptor. Signal 2 — the co-stimulatory signal: CD40 on the B cell binds CD40L on the activated Th cell. CD40–CD40L delivers the most important second signal of B-cell activation.TMU Lecture 7 — Immune Cells Slides 182, 184
4 Central tolerance of B cells — 3 marks+
Three mechanisms operating on self-reactive immature B cells in the bone marrow: clonal deletion (apoptosis), receptor editing (re-rearrangement of the light-chain gene to give a new specificity) and anergy (survival and migration to the periphery in a functionally unresponsive state).TMU Lecture 7 — Immune Cells Slides 168–171
5 B1 cells — 3 marks+
Innate B lymphocytes, 5–10% of all B cells, derived from fetal liver and capable of self-renewal. They reside in the peritoneal cavity, pleural cavity and intestinal mucosal lamina propria, recognise a narrow spectrum (mainly TI antigens and autoantigens), require no T-cell help, show no class switching and no memory, and produce low-affinity multi-reactive IgM including natural antibody against microbial LPS.TMU Lecture 7 — Immune Cells Slides 194–195
6 Plasma cell — 3 marks+
The effector cell into which activated B cells differentiate. Plasma cells lose surface immunoglobulin and become highly specialised for antibody secretion. They do not divide; some travel to the bone marrow and live for years, others die within one or two weeks. The secreted antibody has the same antigen specificity as the original BCR.TMU Lecture 7 — Immune Cells Slides 174, 193
7 Functions of B lymphocytes — 3 marks+
① Production of antibody — neutralisation of toxins and pathogens, complement activation, Fc-receptor-mediated opsonisation, ADCC and type I hypersensitivity, and transport across placenta and mucosa. ② Antigen presentation to T cells — B cells are professional APCs, concentrating antigen via the BCR and presenting it as peptide–MHC class II to Th cells; especially important for soluble antigen. ③ Immune regulation — secretion of IL-6, IL-10 and TNF-α, and suppression by regulatory B cells (Breg).TMU Lecture 7 — Immune Cells Slides 199–210
1B-cell development in the bone marrow passes through four stages: ? cell, ? cell, ? B cell and ? B cell.4 mark(s)
Pro-B first expresses Igα/Igβ; pre-B expresses the pre-BCR; immature B expresses mIgM; mature B expresses mIgM and mIgD.
TMU Lecture 7 — Immune Cells Slide 1672Immature B cells express ? only; mature B cells express ? and ? ; plasma cells express ? .4 mark(s)
This sequence is True/False Q6 — co-expression of mIgM and mIgD is the marker of B-cell maturation.
TMU Lecture 7 — Immune Cells Slide 1793The B-cell co-receptor is a complex of ? , ? and ? .3 mark(s)
⚠️ CD21, not CD20. True/False Q2 prints CD20 in this slot, which is why the statement is false. CD20 is a genuine B-cell marker — the rituximab target — but it is not part of the co-receptor.
TMU Lecture 7 — Immune Cells Slide 180 · confirmed by the student review sheet against the lecture4The three mechanisms of B-cell central tolerance are ? , ? and ? .3 mark(s)
Receptor editing is unique to B cells — a second attempt at the receptor rather than deletion.
TMU Lecture 7 — Immune Cells Slide 1685In the BCR complex, ? binds antigen while ? and ? transduce the signal via ? motifs.4 mark(s)
Structurally identical to the TCR–CD3 arrangement in Unit 7.
TMU Lecture 7 — Immune Cells Slide 1786The second signal for B-cell activation is delivered by ? on the B cell binding ? on the activated Th cell.2 mark(s)
This is MCQ Q10. The question asks for the molecule on B cells, so the answer is CD40 — CD40L is the T-cell side of the same pair.
TMU Lecture 7 — Immune Cells Slide 1847The three main functions of B lymphocytes are ? , ? and ? .3 mark(s)
These three headings are the skeleton of Section V question 5, worth 6 marks and set identically in both papers.
TMU Lecture 7 — Immune Cells Slide 1991The co-receptor of B cell includes CD19/ CD20 /CD81.
FALSE
FALSE. The complex is CD19 / CD21 / CD81. CD20 is a real B-cell molecule — the rituximab target — but it is not part of the co-receptor. A single digit changed turns a true statement false, which is why each CD number must be learnt with its job attached.Past Papers 2019 & 2020, Section IV Q2 — verbatim, both years
2Co-expression of both mIgM and mIgD on the cell surface are the markers for B cell maturation.
TRUE
TRUE. Immature B cells carry mIgM alone; the addition of mIgD marks maturity. Plasma cells then lose surface Ig entirely, because they secrete antibody instead.Past Papers 2019 & 2020, Section IV Q6 — verbatim, both years
3B1 cells require T-cell help to produce antibody.
FALSE
False. B1 cells need no T-cell help, undergo no class switching and generate no memory — they produce low-affinity, multi-reactive IgM. That innate profile is why they are a distractor in MCQ Q11's 'which cell participates in adaptive immunity'.TMU Lecture 7 — Immune Cells Slide 195
4Plasma cells retain surface immunoglobulin and continue to divide.
FALSE
False on both counts. Plasma cells lose surface Ig and do not divide; they are terminally differentiated antibody factories. Some persist in bone marrow for years, others die within one or two weeks.TMU Lecture 7 — Immune Cells Slide 193
5B cells can act as professional antigen-presenting cells.
TRUE
True. They internalise antigen via the BCR or by pinocytosis, process it, and present it as peptide–MHC class II to Th cells. They are especially important for soluble antigen, which macrophages and dendritic cells cannot capture efficiently.TMU Lecture 7 — Immune Cells Slide 209
6CD21 binds complement C3d and is also the receptor for Epstein–Barr virus.
TRUE
True. As CR2 it binds C3d, so complement-tagged antigen engages both BCR and co-receptor at once and lowers the activation threshold. EBV exploits the same receptor — which is exactly why that virus infects B cells.TMU Lecture 7 — Immune Cells Slide 180
1
Please list the functions of B cells, across: cellular immune response, humoral immune response, infection defence, hypersensitivity mediation, anti-tumour effect and allograft rejection.
6 marks
| Role | How B cells contribute |
|---|---|
| Cellular immune response | Act as professional APCs — internalise antigen via the BCR, present it as peptide–MHC class II to Th cells, and express B7 to co-stimulate them; secrete regulatory cytokines (IL-6, IL-10, TNF-α) |
| Humoral immune response | The central role: differentiate into plasma cells and secrete specific antibody of the same specificity as the original BCR |
| Infection defence | Antibody neutralises toxins and viruses, activates complement, and opsonises for phagocytosis; sIgA protects mucosal surfaces and IgG crosses the placenta to protect the newborn |
| Hypersensitivity mediation | Antibody mediates types I, II and III; IgE in particular drives type I |
| Anti-tumour effect | Antitumour antibody supports ADCC and complement-mediated lysis of tumour cells |
| Allograft rejection | Alloantibody contributes to rejection, particularly hyperacute and antibody-mediated rejection |
The examiner supplies the six rows, so the marks are for filling each one — not for an essay. Anchor every row to a mechanism (antibody, presentation, ADCC) rather than a general statement.
Marking guide: 1 mark per row. The humoral and infection-defence rows are the ones that must be right; naming ADCC and alloantibody secures the harder two.
2
Describe the surface molecules of B lymphocytes and their functions.
6 marks
① BCR complex. Membrane Ig (mIg) binds antigen via VH+VL; Igα (CD79a) / Igβ (CD79b) transduce the signal through ITAM motifs.
② Co-receptor. CD19 / CD21 / CD81 — enhances naïve B-cell responsiveness and helps transduce signal 1. CD21 is CR2, the C3d and EBV receptor.
③ Co-stimulatory molecules. CD40 (ligand CD40L on activated Th cells) delivers the most important second signal; B7-1/B7-2 (CD80/CD86) give signal 2 to T cells via CD28; adhesion molecules ICAM-1 and LFA-1 stabilise the contact.
④ Other molecules. CD19 — B-cell marker and CAR-T target; CD20 — B-cell marker and monoclonal-antibody target; CD22 — ITIM, negatively regulates the co-receptor; CD32 — negatively regulates activation and antibody secretion; mitogen receptors PWM-R, LPS-R, SPA-R.
Marking guide: 1.5 marks per group. Distinguishing CD19/CD20/CD21/CD40 by function rather than listing them is what earns full marks.
3
Compare B1 and B2 lymphocytes.
6 marks
| B1 cells | B2 cells | |
|---|---|---|
| Class | Innate | Adaptive |
| Proportion / origin | 5–10%; from fetal liver, self-renewing | Majority; appears late in ontogeny |
| Location | Peritoneal and pleural cavities, intestinal lamina propria | Peripheral lymphoid organs |
| Antigen spectrum | Narrow — mainly TI antigens and autoantigens | Broad — mainly TD antigens |
| T-cell help | Not required | Required |
| Class switching / memory | None / none | Yes / yes |
| Antibody | Low-affinity, multi-reactive IgM; natural antibody against LPS | High-affinity, mainly IgG |
Note the parallel with γδ T cells and TI antigens: the same innate-lymphocyte signature — narrow repertoire, no help needed, IgM only, no memory — recurs three times across this course.
Marking guide: 1 mark per row. The T-help, class-switching and memory rows together define the innate/adaptive distinction and cannot be omitted.