Unit 9 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 of the following is the surface marker profile of a human NK cell?
Answer: C
The profile reads as a sentence: CD3⁻ not a T cell, CD19⁻ not a B cell, CD56⁺ the NK adhesion marker, CD16⁺ FcγRIII — the receptor that lets it perform ADCC.TMU Lecture 7 — Immune Cells Slide 43
2Natural killer cells spare normal host cells because:
Answer: D
Both receptor sets are engaged on a normal cell, but the inhibitory signal — triggered by class I HLA — predominates. The NK cell does not ask “is this foreign?” but “is this still showing me proof that it is mine?”TMU Lecture 7 — Immune Cells Slides 45–46
3“Missing self” recognition by NK cells means that:
Answer: A
Many tumours, and viruses that down-regulate MHC I to hide from CTLs, lose class I expression. The inhibitory signal disappears, activating receptors — NKG2D and the NCRs — win, and the cell is killed. This closes exactly the loophole a CTL leaves open.TMU Lecture 7 — Immune Cells Slide 47
4Killer inhibitory receptors on NK cells bind:
Answer: B
Inhibitory receptors (KIR2DL, KIR3DL, CD94/NKG2A) bind class I HLA; activating receptors bind non-class-I-HLA molecules. Binding IgG Fc is CD16's job, which drives ADCC rather than missing-self killing.TMU Lecture 7 — Immune Cells Slide 45
5A pathogen-associated molecular pattern (PAMP) is best defined as:
Answer: C
PAMPs are conserved because they are essential to being a pathogen — a bacterium cannot abandon its cell wall to escape detection. That is why a small, germline-encoded set of receptors can cover the microbial world. Molecules from damaged host cells are DAMPs; the receptor is the PRR.TMU Lecture 7 — Immune Cells Slide 27
6Which PRR family recognises bacterial LPS and viral nucleic acids?
Answer: D
TLRs 1–9, located on the plasma membrane and in endosomes and lysosomes of DCs, phagocytes, B cells and endothelium. C-type lectins such as the mannose receptor read carbohydrates; scavenger receptors read microbial diacylglycerides; the pentraxin C-reactive protein is a plasma PRR.TMU Lecture 7 — Immune Cells Slide 28
7Neutrophils constitute approximately what proportion of circulating leukocytes, and how long do they function?
Answer: A
They are the majority of circulating leukocytes but extremely short-lived — which is why a rising count (leukocytosis) is such a sensitive early marker of infection, and why the supply must be continuously replenished from bone marrow.TMU Lecture 7 — Immune Cells Slide 33
8Which is the resident macrophage of the liver?
Answer: B
Kupffer cells (liver), microglia (brain), mesangial cells (kidney glomerulus), alveolar macrophages (lung), histiocytes (connective tissue). One lineage, five names.TMU Lecture 7 — Immune Cells Slide 37
9Which receptors allow a macrophage to recognise a microbe WITHOUT antibody or complement?
Answer: C
These are the non-opsonic receptors — PRRs, reading PAMPs directly. FcγR and C3bR/C4bR are the opsonic receptors, which need antibody or complement to have arrived first. The two sets correspond to two eras of the response: PRRs work from minute one, opsonic receptors take over once adaptive immunity has produced antibody.TMU Lecture 7 — Immune Cells Slide 38
10The oxygen-dependent killing system of macrophages comprises:
Answer: D
ROIs (O₂⁻, OH⁻, H₂O₂, ¹O₂) and RNIs (NO). Low pH, lysozyme and defensins are the oxygen-independent system. Perforin and granzymes belong to CTLs and NK cells; C5b–C9 is the complement MAC.TMU Lecture 7 — Immune Cells Slide 41
11Which of the following is classified as an innate-like lymphocyte?
Answer: A
The innate-like lymphocytes (ILLs) are NKT cells, γδ T cells and B1 cells — lymphocytes with rearranged but severely limited repertoires, behaving like innate cells. αβ T cells are the adaptive lymphocyte; neutrophils are classical innate cells, not lymphocytes.TMU Lecture 7 — Immune Cells Slide 22
12NK cells mediate ADCC through which receptor?
Answer: B
CD16 binds the Fc of IgG already coating a target cell, and the NK cell kills it. This is why NK cells appear among the effectors of type II hypersensitivity (antibody bound to a cell surface) but not type I, where IgE is on mast cells rather than on a target cell.TMU Lecture 7 — Immune Cells Slide 44
13Which statement about NK cell antigen recognition is correct?
Answer: C
NK cells carry no antigen-specific receptors and kill tumour and virus-infected cells without antigen stimulation — which is precisely why they are innate and why they are effective immediately, before any adaptive response exists.TMU Lecture 7 — Immune Cells Slide 43
14Damage-associated molecular patterns (DAMPs) are:
Answer: D
The same PRRs that read PAMPs also read DAMPs — so a single receptor system reports both infection and tissue injury. This is why sterile trauma can produce an inflammatory response indistinguishable at first from infection.TMU Lecture 7 — Immune Cells Slide 27
15Whose pattern-recognition theory predicted that innate immunity controls adaptive immunity?
Answer: A
Janeway — of the textbook this course cites. His prediction is what you have already been using: B7 appears on an APC only after a PRR has detected a PAMP, so signal 2 for T-cell activation is innate immunity licensing the adaptive response. Beutler and Hoffmann won the 2011 Nobel Prize for discovering the receptors themselves.TMU Lecture 7 — Immune Cells Slides 29–30
16Why can a virus not escape both CTLs and NK cells by down-regulating MHC class I?
Answer: B
The two killers are deliberately complementary: the CTL kills cells that show the wrong thing (viral peptide on MHC I), while the NK cell kills cells that show nothing at all. There is no level of MHC I expression at which a virus is safe from both.TMU Lecture 7 — Immune Cells Slides 46–47 · Janeway's Immunobiology 10e
1 Pattern recognition receptor (PRR) — 3 marks+
The receptors expressed by innate immune cells, which can recognise certain molecular structures owned by pathogens. Families include Toll-like receptors (TLR1–9, recognising LPS, peptidoglycan and viral nucleic acids), C-type lectin receptors (e.g. mannose receptor), scavenger receptors (e.g. CD36) and pentraxins (e.g. C-reactive protein).TMU Lecture 7 — Immune Cells Slides 26, 28
2 Pathogen-associated molecular pattern (PAMP) — 3 marks+
Highly conserved specific molecular structures expressed by pathogens or their products, which are absolutely distinct from normal host substances and are recognised by the PRRs of innate immune cells. Because PAMPs are essential to the microbe, they cannot be discarded to evade detection — which is why a small germline-encoded receptor set suffices.TMU Lecture 7 — Immune Cells Slide 27
3 Damage-associated molecular pattern (DAMP) — 3 marks+
Substances produced by or released from damaged and dying cells, recognised by the same PRRs that read PAMPs. The innate system therefore reports tissue injury as well as infection.TMU Lecture 7 — Immune Cells Slide 27
4 Natural killer (NK) cell — 3 marks+
An innate lymphoid cell distributed in peripheral blood, liver, lymph node and spleen, carrying no antigen-specific receptors. Human surface markers: CD3⁻ CD19⁻ CD56⁺ CD16⁺. NK cells directly kill tumour cells and virus-infected cells without antigen stimulation and can mediate ADCC through FcγRIII (CD16).TMU Lecture 7 — Immune Cells Slide 43
5 “Missing self” recognition — 3 marks+
The mechanism by which NK cells discriminate targets. NK cells carry both killer activating receptors (binding non-class-I-HLA molecules) and killer inhibitory receptors (binding class I HLA). On a normal cell, class I is expressed normally and the inhibitory signal outweighs activation, so killing is suppressed. On an abnormal cell with reduced class I, inhibition is lost and the activating receptors (NKG2D, NCRs) drive killing.TMU Lecture 7 — Immune Cells Slides 45–47
6 Mononuclear phagocyte system — 3 marks+
Monocytes that leave the blood and mature into tissue macrophages, taking the name of their tissue: Kupffer cells (liver), mesangial cells (kidney glomerulus), microglia (brain), alveolar macrophages (lung), histiocytes (connective tissue). Functions: kill and remove pathogens; kill intracellular bacteria and target cells; participate in and stimulate inflammation; process and present antigen; immunological regulation.TMU Lecture 7 — Immune Cells Slides 36–40
1The human NK cell surface marker profile is ? , ? , ? and ? .4 mark(s)
Not a T cell, not a B cell, NK adhesion marker, and the Fc receptor that enables ADCC.
TMU Lecture 7 — Immune Cells Slide 432NK killer ? receptors bind class I HLA molecules, while killer ? receptors bind non-class-I-HLA molecules.2 mark(s)
On a normal cell the inhibitory signal predominates. Losing class I removes it — “missing self” — and the cell is killed.
TMU Lecture 7 — Immune Cells Slide 453The four PRR families named in the lecture are ? receptors, ? receptors, ? receptors and ? .4 mark(s)
Examples respectively: TLR1–9, mannose receptor, CD36, C-reactive protein.
TMU Lecture 7 — Immune Cells Slide 284Macrophages recognise microbes through non-opsonic receptors — ? , ? and ? — and through opsonic receptors ? and ? .5 mark(s)
Non-opsonic receptors work from the first minute; opsonic receptors only once antibody or complement has arrived. The adaptive response upgrades the macrophage rather than replacing it.
TMU Lecture 7 — Immune Cells Slide 385Macrophage killing uses an oxygen-dependent system of ? and ? , and an oxygen-independent system of ? , ? and ? .5 mark(s)
ROIs are O₂⁻, OH⁻, H₂O₂ and ¹O₂; the RNI is NO; the oxygen-independent pH is 3.5–4.
TMU Lecture 7 — Immune Cells Slide 416The tissue macrophages of liver, kidney glomerulus, brain and lung are called ? , ? , ? and ? .4 mark(s)
Connective tissue's are histiocytes. One lineage, five names.
TMU Lecture 7 — Immune Cells Slide 371NK cells require prior antigen stimulation before they can kill a target cell.
FALSE
False. NK cells have no antigen-specific receptors and kill tumour and virus-infected cells without antigen stimulation. That is exactly what makes them innate and effective from the first hours of an infection.TMU Lecture 7 — Immune Cells Slide 43
2A cell that down-regulates MHC class I becomes more vulnerable to NK cell killing.
TRUE
True — this is missing-self recognition. Losing class I removes the inhibitory signal, so the activating receptors win. It is the trap that closes on viruses which down-regulate MHC I to hide from CTLs.TMU Lecture 7 — Immune Cells Slide 47
3PAMPs are molecules released from damaged host cells.
FALSE
False — those are DAMPs. PAMPs are conserved structures on pathogens, absolutely distinct from normal host substances. Both are read by the same PRRs, which is how one receptor system reports both infection and injury.TMU Lecture 7 — Immune Cells Slide 27
4Neutrophils are long-lived cells that persist in tissue for several weeks.
FALSE
False. Neutrophils function for only 1–2 days and then most die — which is why their numbers must be continuously replenished and why a rising count is such a rapid marker of infection.TMU Lecture 7 — Immune Cells Slide 33
5Microglia are the resident macrophages of the brain.
TRUE
True. The mononuclear phagocyte takes its tissue's name: Kupffer cells in liver, mesangial cells in the renal glomerulus, microglia in brain, alveolar macrophages in lung, histiocytes in connective tissue.TMU Lecture 7 — Immune Cells Slide 37
6γδ T cells, NKT cells and B1 cells are all classified as innate-like lymphocytes.
TRUE
True. All three are lymphocytes with rearranged but severely limited repertoires, behaving like innate cells — fast, stereotyped, no memory. This is precisely why all three appear as wrong answers in MCQ Q11's question about adaptive immunity.TMU Lecture 7 — Immune Cells Slide 22
1
Explain why NK cells kill tumour and virus-infected cells but spare normal host cells.
6 marks
NK cells carry two opposing receptor systems:
| Killer activating receptors | Killer inhibitory receptors | |
|---|---|---|
| Examples | KIR2DS, KIR3DS; CD94/NKG2C, NKG2D; NCRs (NKp46, NKp30, NKp44) | KIR2DL, KIR3DL; CD94/NKG2A |
| Bind | Non-class-I-HLA molecules | Class I HLA molecules |
On a normal cell, class I HLA is expressed normally, so the inhibitory receptors are engaged and their signal outweighs the activating signal — killing is suppressed.
On an abnormal cell — many tumours, and cells infected by viruses that down-regulate MHC I — class I expression is lost or reduced. The inhibitory signal disappears, the activating receptors (NKG2D and the NCRs) predominate, and the target is killed. This is “missing self” recognition.
NK cells can additionally kill by ADCC: FcγRIII (CD16) binds IgG already coating a target cell.
Significance: a virus that switches off MHC I to escape CD8⁺ CTLs thereby exposes itself to NK cells — the two killers are complementary.
Marking guide: 2 marks for naming both receptor systems and their ligands, 2 for the normal vs abnormal cell comparison, 1 for naming missing-self, 1 for ADCC or the CTL-complementarity point.
2
Describe the characteristics and functions of macrophages.
6 marks
Origin and distribution. HSC → myeloid progenitor → pre-monocyte → blood monocyte → tissue macrophage. Tissue names: Kupffer cells (liver), mesangial cells (kidney glomerulus), microglia (brain), alveolar macrophages (lung), histiocytes (connective tissue).
Recognition receptors. Non-opsonic (PRR) — mannose receptor, scavenger receptor, Toll-like receptor. Opsonic — FcγR and C3bR/C4bR.
Killing mechanisms. Oxygen-dependent — reactive oxygen intermediates (O₂⁻, OH⁻, H₂O₂, ¹O₂) and reactive nitrogen intermediates (NO). Oxygen-independent — low pH (3.5–4), lysozyme, defensins.
Functions. ① Kill and remove pathogens. ② Kill intracellular bacteria and target cells (tumour cells, virus-infected cells). ③ Participate in and stimulate inflammation. ④ Process and present antigen. ⑤ Immunological regulation.
Marking guide: 1.5 marks per heading. The five functions are the core; naming both receptor classes and both killing systems secures full marks.
3
What are PRRs and PAMPs, and why is this recognition system effective?
6 marks
PRR — pattern recognition receptors: the receptors expressed by innate immune cells which recognise certain molecular structures owned by pathogens. Families: Toll-like receptors (TLR1–9; LPS, peptidoglycan, viral nucleic acids), C-type lectin receptors (mannose receptor; fungal and mycobacterial carbohydrate), scavenger receptors (CD36), pentraxins (C-reactive protein).
PAMP — pathogen-associated molecular patterns: highly conserved structures expressed by pathogens or their products, absolutely distinct from normal host substances. DAMPs are the equivalent signals released from damaged and dying host cells.
Why it works. PAMPs are conserved because they are essential to the microbe — a bacterium cannot discard its cell wall to evade detection. So a small, germline-encoded set of receptors covers whole classes of pathogen, is available immediately without any prior exposure, and cannot be escaped by mutation as an antigenic epitope can.
Link to adaptive immunity. PRR engagement induces B7 expression on APCs, supplying signal 2 for T-cell activation — Janeway's prediction that innate immunity controls adaptive immunity.
Marking guide: 2 marks for each definition with examples, 2 for the reasoning about conservation and immediacy. The link to signal 2 is the discriminating point.