✓✗ True / False Trainer

True. Slide 42 of the lecture states it directly: broadly, the different types of immune response fall into two categories, innate (non-adaptive) and adaptive (acquired). Appeared unchanged as Section IV question 4 in both years.Past Papers 2019 & 2020, Section IV Q4 — verbatim, both years→ read the unit

False. Adaptive immunity is acquired — it requires antigen exposure to be initiated, which is precisely why it takes 4–5 days to become effective on a first encounter. Innate immunity is the arm that works without prior exposure.TMU Lecture 1 (Prof. Shan Yu Fung) Slide 63→ read the unit

False. The thymus is a central (primary) lymphoid organ along with bone marrow. The peripheral organs are lymph node, spleen and MALT.Janeway's Immunobiology 10e, §1-14→ read the unit

False. Memory is a defining feature of adaptive immunity. Innate immunity reacts in essentially the same way to repeated infections — the hundredth exposure looks like the first.TMU Lecture 1 (Prof. Shan Yu Fung) Slides 45, 58→ read the unit

False, and this is the whole point of the theory. The receptor exists before the antigen arrives, generated at random. The antigen selects the lymphocytes that already fit it and drives them to proliferate. Instructional theories were the rival hypothesis, and they lost.Janeway's Immunobiology 10e, §1-12→ read the unit

True. Passive immunity transfers pre-formed antibody or lymphocytes, so protection begins at once — but the recipient's own immune system was never engaged, so nothing is remembered and protection wanes as the transferred material is cleared. This is why antitoxin is given in acute diphtheria and a vaccine is not.TMU Lecture 1 (Prof. Shan Yu Fung) Slide 72→ read the unit

False. Mitogens activate lymphocytes non-specifically and polyclonally — which is precisely why they are classed as non-specific stimulators alongside superantigens and adjuvants. Every other word in the sentence is correct, so the trap is the adverb. Set in both papers, unchanged.Past Papers 2019 & 2020, Section IV Q1 — verbatim, both years→ read the unit

False. That is the definition of a hapten — it lacks immunogenicity. It will bind antibody that already exists, but it cannot induce antibody until a carrier supplies the missing bulk and T-cell epitopes.TMU Lecture 2 (Lei Zhi) Slide 17→ read the unit

True. A conformational epitope is made of residues that are distant in the sequence and only adjacent because of folding. Unfold the protein and the epitope ceases to exist. Linear epitopes survive, and some previously buried ones are newly exposed.TMU Lecture 2 (Lei Zhi) Slide 26→ read the unit

False. TI antigens give IgM only, with no class switching and no memory. This is the clinical reason plain polysaccharide pneumococcal vaccine protects infants poorly, and why the conjugate version — which converts it into a TD antigen — was developed.TMU Lecture 2 (Lei Zhi) Slide 49→ read the unit

False. Size helps but is not sufficient — complexity is also required. Gelatin exceeds 100 kD and is a poor immunogen because it is a monotonous straight-chain polymer; adding about 2% tyrosine makes it much stronger.TMU Lecture 2 (Lei Zhi) Slide 41→ read the unit

False. Superantigens bypass processing entirely, clamping intact MHC class II to the TCR from the outside. No processing, no MHC restriction, and polyclonal activation of a large fraction of T cells — the mechanism behind toxic shock syndrome.TMU Lecture 2 (Lei Zhi) Slide 67→ read the unit

False — the relationship runs the other way. Antibodies are immunoglobulins, but immunoglobulins are not always antibodies. A membrane-bound BCR that has not yet met its antigen, or a myeloma protein of irrelevant specificity, is immunoglobulin without antibody function.TMU Lecture 3 (Lei Zhi) Slides 5, 7→ read the unit

False. Both light-chain types occur across all five classes, but any single immunoglobulin molecule carries only one type. Its two light chains are identical, as are its two heavy chains.TMU Lecture 3 (Lei Zhi) Slide 12→ read the unit

True. The hinge is present only in γ, α and δ chains. IgM and IgE instead have a fourth C_H domain occupying that position — which is why the two facts are best learnt as a pair.TMU Lecture 3 (Lei Zhi) Slides 31–32→ read the unit

True. Pepsin cuts below the inter-heavy-chain disulfides, so the two arms remain joined and the fragment stays bivalent. It cannot fix complement or bind Fc receptors, because the Fc is destroyed — but binding and cross-linking are intact.TMU Lecture 3 (Lei Zhi) Slide 43→ read the unit

False. Antigen binding is entirely a V-region function — V_H + V_L, six CDRs. The Fc is constant region only, and carries effector functions: complement fixation, Fc-receptor binding and placental transfer.TMU Lecture 3 (Lei Zhi) Slides 20, 42→ read the unit

True, via placental Fc receptors, and mainly subclasses IgG1, IgG3 and IgG4. It is the basis of natural passive immunity in the newborn — and of haemolytic disease of the newborn when the maternal antibody is anti-D.TMU Lecture 3 (Lei Zhi) Slides 73, 78→ read the unit

False. The lecture states it explicitly: free antibody cannot bind or activate complement. The C1q site in C_H2 is exposed only after antigen binding shifts the molecule from a T shape to a Y shape — the geometric safety catch that keeps your circulating IgG inert.TMU Lecture 4 (Juan Li) Slides 16, 21→ read the unit

True. C1 must engage at least two antibody molecules at once. A single pentameric IgM presents several Fc regions together and can do it alone; IgG requires two separate molecules to land close enough on the surface.TMU Lecture 4 (Juan Li) Slides 20, 25, 28→ read the unit

False. Both are antibody-independent and belong to innate immunity — which is why they operate in the early stage of an infection, before an adaptive response exists. Only the classical pathway needs antibody.TMU Lecture 4 (Juan Li) Slide 71→ read the unit

True. MASP-2 does the job of C1s, cleaving C4 and C2, so the lectin pathway generates C4b2a and C4b2a3b — identical to the classical pathway. Only the recognition step differs: MBL binds sugar where C1q binds antibody.TMU Lecture 4 (Juan Li) Slides 58, 71→ read the unit

False. Those are the anaphylatoxins — small fragments released into the fluid phase to drive inflammation. The MAC is built from the 'b' and terminal components: C5b, C6, C7, C8, C9.TMU Lecture 4 (Juan Li) Slide 59 · Janeway's Immunobiology 10e, §2-14→ read the unit

True. A somatic mutation in the GPI-anchor pathway strips both DAF (CD55) and CD59 from the red-cell surface at once, leaving the cells defenceless against the constantly ticking alternative pathway. It is the clearest demonstration that the alternative pathway spares host cells only because host cells are protected.Janeway's Immunobiology 10e, §2-16, §2-17→ read the unit

FALSE. IL-4, IL-5 and IL-10 are the Th2 profile. Th1 secretes IL-2, IFN-γ and TNF. ⭐ In the 2020 paper the same sentence appears with Th2 in place of Th1 — and the answer becomes TRUE. This is the only item on the entire paper whose answer changes between the two years.Past Paper 2019, Section IV Q3→ read the unit

TRUE — the Th2 profile, along with IL-6 and IL-13. Compare with the statement above: one word changed and the correct answer inverted. Anyone who memorised the 2019 key without learning the profiles scores 11 out of 12 and never finds out why.Past Paper 2020, Section IV Q3→ read the unit

False. The five attributes are pleiotropism, redundancy, synergy, antagonism and cascade induction. Specificity belongs to the antigen receptors. Pleiotropism and redundancy between them make specificity structurally impossible: one cytokine does many things, and many cytokines do the same thing.Past Papers 2019 & 2020, Section III Q15 · TMU Lecture 5 (Juan Li) Slide 14→ read the unit

False. Cytokine secretion is a brief, self-limited event: they are not stored preformed, but synthesised on demand and secreted immediately. This is why cytokine effects are normally confined in time as well as in space.TMU Lecture 5 (Juan Li) Slide 10→ read the unit

True — IL-6 is made by macrophages, endothelial cells and T cells alike. The converse is also true: one Th cell makes IL-2, IL-4, IL-5, IL-10 and IFN-γ. This promiscuity is precisely why the older names (monokine, lymphokine) were abandoned in favour of classification by function.TMU Lecture 5 (Juan Li) Slide 10→ read the unit

False. IFN-γ is type II, produced by activated T cells and NK cells, and acts mainly to activate macrophages. Type I is IFN-α and IFN-β, produced by dendritic cells and infected cells, and is the antiviral arm.TMU Lecture 5 (Juan Li) Slide 20→ read the unit

True — and this is why the system exists. Once hybridomas made monoclonal antibodies easy to produce, many laboratories were naming the same surface molecules differently; grouping antibodies into numbered clusters solved it.TMU Lecture 6 — CDs and CAMs Slide 4→ read the unit

False. CD16 (FcγRIII) is on NK cells, macrophages and neutrophils, where it mediates ADCC and the uptake of antibody-coated pathogens. The B-cell IgG Fc receptor is CD32. ⚠️ The deck's printed table appears to show CD16 under B cells; that is a typesetting artefact and is corrected here against Janeway's.Janeway's Immunobiology 10e on CD16/FcγRIII→ read the unit

False — that is the selectins. Integrins act later, and only after chemokine signalling has switched them to a high-affinity state; they provide the firm adhesion that arrests the cell. A strong bond formed at full flow velocity would tear, which is why the weak carbohydrate bond has to come first.TMU Lecture 6 — CDs and CAMs Slides 9, 12→ read the unit

True, and the two descriptions are the same fact from two angles: CD4 and CD8 grip the MHC molecule on the antigen-presenting cell and hold the contact together while the TCR reads the peptide. The lineage marker is the adhesion function.TMU Lecture 6 — CDs and CAMs Slides 6, 14→ read the unit

False. Naïve T cells home to secondary lymphoid tissues, where antigen is brought to them — there would be no point sending a cell that has never met its antigen to a particular tissue. Only after activation do effector T cells acquire receptors for mucosal or cutaneous addressins.TMU Lecture 6 — CDs and CAMs Slide 16→ read the unit

False — it is characteristically high. The neutrophils are produced normally but cannot adhere firmly and so cannot leave the vessel, accumulating in the blood instead. The same mechanism explains the absence of pus and the delayed umbilical cord separation.Janeway's Immunobiology 10e — Case Study: Leukocyte Adhesion Deficiency→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

FALSE. That describes class I. Class II is restricted to dendritic cells, macrophages and B cells plus thymic stroma. The statement is true of the wrong class — the neatest kind of trap, and it appears unchanged in both papers.Past Papers 2019 & 2020, Section IV Q12 — verbatim, both years→ read the unit

False. β2-microglobulin associates with the class I α chain but is not MHC-encoded and forms no part of the peptide groove — which is exactly why class I must build its cleft from α1 + α2 of its single MHC chain.TMU Lecture 10 — MHC Slides 11, 26→ read the unit

False — MHC is co-dominant with no allelic exclusion; both maternal and paternal products appear in the same cell. Allelic exclusion belongs to antigen receptors, where one lymphocyte must have one specificity.TMU Lecture 10 — MHC Slide 18→ read the unit

False. Class I is on all nucleated cells, and mature red cells have no nucleus — this is MCQ Q7. It is also why transfusion compatibility runs on ABO and Rh rather than HLA.Past Papers 2019 & 2020, Section III Q7→ read the unit

True. Each MHC allele requires only a couple of specific anchor residues at fixed positions; everything between them is unconstrained. MHC is deliberately low-specificity and high-breadth — the specificity is supplied afterwards by the TCR reading the peptide–MHC combination.TMU Lecture 10 — MHC Slide 29→ read the unit

True — C4, C2 and factor B, together with TNF and HSP70. A single genetic region therefore carries both the peptide-display system and several of the effector molecules that act on what it reveals.TMU Lecture 10 — MHC Slides 7, 9→ read the unit

True — which is why the DC is called the initiator of the immune response and why it is the answer to MCQ Q8. It alone expresses MHC and co-stimulatory molecules constitutively, so it can deliver signal 1 and signal 2 together without needing prior activation.TMU Lecture 8 — Antigen Presenting Cells Slides 11, 14→ read the unit

False — the reverse. Uptake falls from ++++ to + on maturation, while presentation rises from + to ++++. The DC stops sampling and starts reporting, because it cannot be in the peripheral tissue and the lymph node at the same time.TMU Lecture 8 — Antigen Presenting Cells Slide 11→ read the unit

False. All nucleated cells present on class I — any cell can be infected and must be able to report its own cytoplasm. The restriction to professional APCs applies to class II.TMU Lecture 8 — Antigen Presenting Cells Slide 18 · Unit 10→ read the unit

False. T cells recognise only antigen that has been processed and presented on MHC. B cells are the ones that read native antigen directly through the BCR — and that difference is the entire reason APCs exist.TMU Lecture 8 — Antigen Presenting Cells Slide 3→ read the unit

True. The BCR captures and concentrates the cell's own specific antigen, giving Ig-mediated uptake rated ++++. Macrophages and DCs cannot capture soluble antigen efficiently — so the B cell fills exactly that gap.TMU Lecture 8 — Antigen Presenting Cells Slide 14 · TMU Lecture 7 — Immune Cells Slide 209→ read the unit

False — they are non-professional APCs, along with fibroblasts, thymic and thyroid epithelium, glial cells and pancreatic β cells. They can be induced to express class II under inflammatory conditions but do not do so constitutively.TMU Lecture 8 — Antigen Presenting Cells Slide 5→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

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→ read the unit

False. IgE does not fix complement — one of its listed properties. Its mechanism is entirely FcεRI-mediated mast-cell degranulation, which is also why complement plays no part in type I.TMU Lecture 11 — Hypersensitivity Slide 35→ read the unit

False. The first exposure sensitizes — IgE is made and binds FcεRI, silently. It is the second exposure that cross-links and causes degranulation.TMU Lecture 11 — Hypersensitivity Slides 42–43→ read the unit

True — half of True/False Q11. Th2 secretes IL-4, which drives B-cell class switching to IgE. The other half, Th1 driving type IV, is also true.Past Papers 2019 & 2020, Section IV Q11→ read the unit

False. One allergen must bridge two adjacent IgE molecules to cross-link the receptors — which is why an allergen must be at least bivalent, and why desensitization works.TMU Lecture 11 — Hypersensitivity Slide 43→ read the unit

False. Eosinophils participate in the late-phase reaction and down-regulate type I hypersensitivity through some of the mediators they synthesise and release.TMU Lecture 11 — Hypersensitivity Slide 38→ read the unit

True. Long intervals (5–7 days) of small allergen doses shift the B-cell response toward IgG, which then blocks allergen before it reaches mast-cell IgE. Desensitization, at 20–30 minute intervals, works differently — by exhausting the mediators.TMU Lecture 11 — Hypersensitivity Slide 59→ read the unit

TRUE. All three effector routes: complement-mediated lysis, opsonised phagocytosis by macrophages, and ADCC by NK cells. Contrast MCQ Q17, where NK cells are the answer to “not involved in type I” — because ADCC needs IgG on a target cell, which type I does not have.Past Papers 2019 & 2020, Section IV Q10 — verbatim, both years→ read the unit

TRUE. Rhogam binds fetal Rh antigen and clears those cells before the mother's immune system can respond, preventing B-cell activation and memory-cell generation. No memory, no secondary IgG response, no disease in the next pregnancy.Past Papers 2019 & 2020, Section IV Q7 — verbatim, both years→ read the unit

False. IgM cannot cross the placenta — it is a 900 kD pentamer. That is exactly why the first Rh⁺ baby is spared: the mother's primary response is IgM. The disease requires the IgG of a secondary response.TMU Type II Hypersensitivity deck (Yu Chunyan) Slides 18–19→ read the unit

False. In type II the antigen is on a cell surface. Soluble circulating antigen forming immune complexes defines type III — and that difference is the whole distinction between the two.TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 8→ read the unit

False — by IgM. Anti-A and anti-B are natural antibodies against carbohydrate (TI) antigens, so no class switching occurs and they remain IgM. Being IgM they activate complement extremely efficiently, causing immediate intravascular haemolysis.TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 17→ read the unit

True, and that is precisely why it causes brain damage — it can enter brain tissue. Phototherapy breaks it down, and exchange transfusion is performed primarily to remove it.TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 22→ read the unit

TRUE — both halves. Th1 secretes IFN-γ, which activates macrophages and drives the delayed reaction; Th2 secretes IL-4, which drives class switching to IgE and so drives type I. The same Unit 5 knowledge answers this and the Th1/Th2 True/False trap.Past Papers 2019 & 2020, Section IV Q11 — verbatim, both years→ read the unit

False — and this is one of its three defining properties. Type IV is purely cell-mediated: CD4⁺ Th1 and CD8⁺ CTL, with macrophages recruited. The 24–72 hour delay is the clinical evidence of it.TMU Type III & IV Hypersensitivity deck Slide 20→ read the unit

False. Large complexes are cleared rapidly by the phagocyte system and cause no damage. It is the medium-sized complexes that deposit and cause disease.TMU Type III & IV Hypersensitivity deck Slide 4→ read the unit

False — a dangerous assumption. A negative test may also mean the vaccine has lost efficacy, or that the patient is immunodeficient and cannot mount the T-cell response. The test measures the response, not the organism.TMU Type III & IV Hypersensitivity deck Slide 29→ read the unit

False, and the deck says so explicitly: the term hypersensitivity is somewhat misleading. DTH is an important effector form of cell-mediated immunity — in essence, inflammation — and it is how intracellular organisms such as tuberculosis are contained. The granuloma is both tissue damage and successful containment.TMU Type III & IV Hypersensitivity deck Slide 39→ read the unit

True. Large amounts of horse antiserum provoke antibody while the horse protein is still circulating; antigen and antibody meet in the blood at the mid-range ratio, forming medium-sized complexes. Symptoms — fever, weakness, vasculitis — appear 1–2 weeks later.TMU Type III & IV Hypersensitivity deck Slide 11→ read the unit

False — direct agglutination detects antigen, as in ABO blood typing, where known anti-A and anti-B sera identify the antigen on the patient's red cells. Indirect agglutination detects antibody.TMU Lecture 12 — Immunoassay (Yu Chunyan) Slide 18→ read the unit

True. Every technique in the unit is a way of making that invisible binding event visible and then countable — by clumping, precipitating, or attaching a label that generates a signal.TMU Lecture 12 — Immunoassay (Yu Chunyan) Slide 14→ read the unit

False — which is precisely why immune cells are evaluated on two separate axes, number and function. Functional tests such as the lymphocyte transformation test exist for exactly this reason.TMU Lecture 12 — Immunoassay (Yu Chunyan) Slide 10→ read the unit

FALSE — and this matters. Slide 3 gives 6 definitions (18), 56 blanks at 0.5 each (28), 20 single choices (20), 10 MULTIPLE choices (10) and 4 brief answers (24). The past papers instead have 20 blanks, a 12-mark true/false section, and five brief answers. A multi-answer MCQ section appears in neither past paper. Prepare the content, not the format.TMU Lecture 12 — Immunoassay (Yu Chunyan) Slide 3→ read the unit

True, and it is the living demonstration of Unit 1's claim about the thymus. Such mice cannot reject skin grafts, which is why they are used to grow human tumour xenografts.TMU Lecture 12 — Immunoassay (Yu Chunyan) Slide 13→ read the unit

TRUE — the lecture's definition verbatim. The exam statement is the slide, so learning the definition answers the question exactly.Past Papers 2019 & 2020, Section IV Q8 — verbatim, both years→ read the unit

TRUE — the four stated criteria. 'Practical considerations' covers cost, stability and ease of administration, which is why the DNA vaccine's freedom from a cold chain is such an advantage in the field.Past Papers 2019 & 2020, Section IV Q9 — verbatim, both years→ read the unit

False. The response is primarily humoral, because the injected protein is exogenous antigen processed by the MHC class II pathway. It never reaches the cytosol, so no MHC class I presentation and no CTL response occurs — which is exactly the gap DNA vaccines were designed to fill.TMU Lecture 13 — Immunotherapy (Yu Chunyan) Slide 10→ read the unit

False — one of their principal advantages is that they are highly stable and resistant to high temperature, so no cold chain is necessary. That is a decisive practical benefit in field conditions.TMU Lecture 13 — Immunotherapy (Yu Chunyan) Slide 14→ read the unit

True. Freund's complete adjuvant is far too inflammatory for human use and is restricted to research animals. Modern adjuvants under development are TLR agonists such as CpG.TMU Lecture 13 — Immunotherapy (Yu Chunyan) Slide 18→ read the unit

False. They kill nothing. They remove an inhibitory signal — typically PD-L1 on the tumour engaging PD-1 on infiltrating T cells — restoring a T-cell response the patient already had. That is also why the toxicity is autoimmune rather than cytotoxic.TMU Lecture 13 — Immunotherapy (Yu Chunyan) Slides 23–24→ read the unit