✏️ Fill in the Blanks
Section II · 20% · 1 mark per blank · 107 items from the units built so far
Twenty marks, one per blank — the highest mark-per-second section on the paper, and one your other subjects never test. The same seven slots recur each year with small variations, so drill the set rather than the exact gap: in 2019 the paper gave you immune defence and asked for two functions; in 2020 it asked for all three.
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Unit 1 · Overview of Immunology
1Cellular immunity is mediated by ? cell. Humoral immunity is mediated by ? cell.2 mark(s)
The most reliably repeated item on the paper — question 1 of Section II in both years, word for word. T for thymus (cellular); B for bone marrow, and B makes antibodies (humoral). Two free marks; the only way to lose them is to write them in the wrong order.
Past Papers 2019 & 2020, Section II Q1 — verbatim, both years→ read the unit2The functions of immune systems include ? , ? and ? .3 mark(s)
The 2019 paper gave immune defence and asked for two blanks; the 2020 paper asked for all three. Learn the set rather than the gap. Each has a matching disease on failure: defence → immunodeficiency or hypersensitivity; homeostasis → autoimmunity; surveillance → tumours.
Past Paper 2020, Section II Q2 (2019 gave 'immune defence')→ read the unit3Peripheral immune organs include ? , ? and ? .3 mark(s)
MALT is mucosa-associated lymphoid tissue — the lymphoid tissue of the gut, respiratory and urogenital tracts. In 2020 the paper supplied spleen and asked only for the other two. Do not write thymus or bone marrow: those are the central organs.
Past Paper 2019, Section II Q3 (2020 supplied 'spleen')→ read the unit4The two central (primary) immune organs are ? and ? .2 mark(s)
The counterpart to the peripheral-organ question above, and worth rehearsing in both directions since the examiner has asked the peripheral half twice. Janeway's: “The central lymphoid organs are the bone marrow and the thymus.”
Janeway's Immunobiology 10e, §1-14 · TMU Lecture 1 (Prof. Shan Yu Fung) Slide 81→ read the unit5Innate immunity recognises antigen using ? receptors, whereas adaptive immunity uses ? and ? .3 mark(s)
The recognition row of the innate-versus-adaptive comparison table, which is Section V question 1. PRRs are germline-encoded and read broad molecular patterns; TCR and BCR are generated by gene rearrangement and read individual epitopes.
TMU Lecture 1 (Prof. Shan Yu Fung) Slide 63 · Janeway's Immunobiology 10e, §1-5→ read the unitUnit 2 · Antigen
6An antigen molecule generally possesses two properties: ? and ? .2 mark(s)
Immunogenicity = the ability to induce a response; antigenicity (immunoreactivity) = the ability to be bound by that response's products. A hapten has the second without the first.
TMU Lecture 2 (Lei Zhi) Slide 12 · phrasing confirmed by the student review sheet→ read the unit7Using a specific hapten coupled to a ? , a specific antibody can be produced.1 mark(s)
The carrier is usually a protein. It supplies the bulk and the T-cell epitopes the hapten lacks, so T-cell help can be recruited and antibody made against the hapten itself. Conjugate vaccines exploit exactly this.
TMU Lecture 2 (Lei Zhi) Slide 16→ read the unit8Immunologically active structures of an antigen that bind to antigen receptors on lymphocytes or to secreted antibodies are called ? or ? .2 mark(s)
The two words are interchangeable. TMU uses both, and the 2020 paper set Epitope as a Section I definition.
TMU Lecture 2 (Lei Zhi) Slide 23→ read the unit9The epitopes recognised by the TCR are called ? epitopes, and those recognised by the BCR are called ? epitopes.2 mark(s)
T-cell epitopes are linear peptides that must be presented on MHC; B-cell epitopes are usually conformational and are read directly off the native antigen surface.
TMU Lecture 2 (Lei Zhi) Slides 28–30→ read the unit10TD antigens induce B-cell activation only when specific ? cells are present.1 mark(s)
That is what 'thymus-dependent' means. Without T help a protein antigen cannot drive class switching, affinity maturation or memory — which is why conjugating a polysaccharide to a protein carrier transforms the response.
TMU Lecture 2 (Lei Zhi) Slide 50→ read the unit11The three features of a superantigen are ? activation, ? antigen processing, and ? MHC restriction.3 mark(s)
All three follow from one structural fact: the superantigen binds the outside of MHC II and the outside of the TCR, so the peptide groove is irrelevant.
TMU Lecture 2 (Lei Zhi) Slide 67→ read the unitUnit 3 · Immunoglobulin
12The H chains of the five classes of Ig are ? , ? , ? , ? and ? .5 mark(s)
γ→IgG, α→IgA, μ→IgM, ε→IgE, δ→IgD. Do not slip κ or λ into this list — those are the light chains, and MCQ Q9 is built on exactly that confusion.
TMU Lecture 3 (Lei Zhi) Slide 12 · phrasing confirmed by the student review sheet→ read the unit13L chains of Ig may be divided into ? and ? isotypes.2 mark(s)
Both types occur in all five classes, but any one immunoglobulin molecule carries only one type — never one κ and one λ.
TMU Lecture 3 (Lei Zhi) Slides 12, 31→ read the unit14Ig that has the largest molecular weight is ? ; Ig which consists of a dimer structure is ? ; Ig which mediates type I hypersensitivity is ? ; Ig which appears in the early stage of infection is ? .4 mark(s)
The 2019 wording. In 2020 the first clause became “Ig that mediates mucosal immunity is ___”, answer SIgA. Four marks, and they are pure superlative recall — learn the class table as a set of superlatives.
Past Paper 2019, Section II Q5 (2020 varies the first clause)→ read the unit15The most abundant class of Ig in serum is ? ; the Ig present at mucous membrane surfaces is ? ; the Ig that crosses the placenta is ? .3 mark(s)
IgG is about 80% of serum Ig and is the only class that crosses the placenta. sIgA is the mucosal antibody — it is a dimer with a J chain and a protective secretory piece.
TMU Lecture 3 (Lei Zhi) Slides 77–83→ read the unit16Digestion of IgG by papain yields two identical ? fragments and one ? fragment.2 mark(s)
Papain cuts on the N-terminal side of the inter-heavy-chain disulfide bonds, so the arms come away separately. Pepsin cuts on the other side and yields one bivalent F(ab′)₂ plus functionless pFc′.
TMU Lecture 3 (Lei Zhi) Slide 40→ read the unit17The binding site for C1q is located in the ? domain of IgG and the ? domain of IgM.2 mark(s)
IgG binds C1q through CH2 (subclasses IgG1, IgG2, IgG3); IgM binds through CH3. Both require antigen to have been bound first — the shape change exposes the site.
TMU Lecture 3 (Lei Zhi) Slide 60 · confirmed by the student review sheet against the lecture→ read the unit18The Ig classes that possess subclasses are ? and ? .2 mark(s)
IgG1–IgG4 and IgA1–IgA2. Light chains have subtypes as well — κ1/κ2 and λ1/λ2.
TMU Lecture 3 (Lei Zhi) Slides 28, 50→ read the unit19The most opsonising Ig isotype is ? .1 mark(s)
Phagocytes carry Fcγ receptors, so IgG-coated microbes are bound and ingested far more efficiently. Opsonisation is one of the five Fc-mediated functions.
TMU Lecture 3 (Lei Zhi) Slide 62→ read the unit20By immunising animals we obtain ? antibodies, whereas ? antibodies are produced by a single clone of B lymphocytes.2 mark(s)
An antigen carries many epitopes, so immunisation recruits many B-cell clones and the antiserum is a mixture. A monoclonal antibody comes from one clone via the hybridoma method and recognises one epitope.
TMU Lecture 3 (Lei Zhi) Slides 91, 93→ read the unitUnit 4 · The Complement System
21In the classical pathway of complement activation, C3 convertase is ? ; C5 convertase is ? ; MAC is ? .3 mark(s)
⚠️ Write C4b2a, not C4b2b. The circulated student review sheets give C4b2b, but TMU's own Lecture 4 deck writes C4b2a seventeen times and C4b2b never; Janeway's confirms that C2a is the larger, active fragment of C2.
Past Paper 2019, Section II Q4 — set for the classical pathway in 2019→ read the unit22In the alternative pathway of complement activation, C3 convertase is ? ; C5 convertase is ? ; MAC is ? .3 mark(s)
The 2020 paper asked the same question about the alternative pathway instead of the classical — so learn both rows. In every pathway the C5 convertase is simply the C3 convertase with a C3b added.
Past Paper 2020, Section II Q4 — set for the alternative pathway in 2020→ read the unit23Complement C1 is a large protein complex composed of ? , ? and ? .3 mark(s)
One C1q with two molecules each of C1r and C1s. C1q has 18 polypeptide chains forming six collagen-like arms, which is how it engages two antibody Fc regions at once — the minimum needed for activation.
Past Paper 2019, Section II Q6→ read the unit24The three pathways of complement activation are ? , ? and ? .3 mark(s)
Classical is antibody-dependent; alternative and lectin are antibody-independent and belong to innate immunity, acting earlier in infection.
TMU Lecture 4 (Juan Li) Slide 9 · phrasing confirmed by the student review sheet→ read the unit25The initiating substance of the classical pathway is the ? complex; of the alternative pathway, components on the ? surface; of the lectin pathway, ? residues.3 mark(s)
Three different recognition events converging on the same amplifier. Only the classical route needs a prior adaptive immune response.
TMU Lecture 4 (Juan Li) Slide 71→ read the unit26The alternative pathway C3 convertase is stabilised by ? , also known as factor ? .2 mark(s)
Without properdin the C3bBb complex is short-lived. Stabilised, it drives the amplification loop that generates up to 90% of all deposited C3b regardless of which pathway started the reaction.
TMU Lecture 4 (Juan Li) Slides 41, 43→ read the unit27The membrane attack complex is composed of complement components ? through ? , and the component that polymerises to form the pore is ? .3 mark(s)
C5b binds the surface, C6 joins, C7 inserts into the bilayer, C8 follows, and several C9 molecules polymerise into the channel.
TMU Lecture 4 (Juan Li) Slides 59–64→ read the unitUnit 5 · Cytokines
28Cytokines secreted by Th1 cells include ? , ? and ? .3 mark(s)
⚠️ IFN-γ and IL-2 are beyond doubt. For the third, TMU Lecture 7 slide 139 writes TNF-α, the circulated student sheets write TNF-β, and Janeway's shows Th1 cells release both TNF-α and lymphotoxin (which is TNF-β). Write TNF, or TNF-α if a specific form is required — that is your department's own wording.
Past Paper 2020, Section II Q7 · TMU Lecture 7 — Immune Cells Slide 139→ read the unit29Cytokines secreted by Th2 cells include ? , ? and ? .3 mark(s)
Also IL-6 and IL-13. Th2 makes neither IL-2 nor IFN-γ. This exact set is what makes the True/False trap work — IL-4, IL-5, IL-10 is a Th2 profile, so the 2019 statement attributing it to Th1 is false and the 2020 statement attributing it to Th2 is true.
TMU Lecture 7 — Immune Cells Slide 139→ read the unit30The five attributes of cytokines are ? , ? , ? , ? and ? .5 mark(s)
Cytokines notably do not possess specificity — that is the property MCQ Q15 asks about.
TMU Lecture 5 (Juan Li) Slides 14, 16→ read the unit31Cytokines may act in three ways: ? action on the same cell, ? action on a nearby cell, and ? action at a distance through the circulation.3 mark(s)
Paracrine is the usual mode, which is why cytokines are described as acting locally in contrast to hormones.
TMU Lecture 5 (Juan Li) Slide 12→ read the unit32Type I interferons are ? and ? ; type II interferon is ? .3 mark(s)
Type I is produced by dendritic cells and infected cells and is antiviral; type II is produced by activated T cells and NK cells and mainly activates macrophages.
TMU Lecture 5 (Juan Li) Slide 20→ read the unit33Differentiation of Th0 into Th1 is induced by ? and ? , while differentiation into Th2 is induced by ? .3 mark(s)
Each lineage then secretes the cytokine that drives its own differentiation and inhibits the other, so the commitment becomes self-locking.
TMU Lecture 7 — Immune Cells Slide 144→ read the unit34The six classes of cytokine are ? , ? , ? , ? , ? and ? .6 mark(s)
The interleukins now run from IL-1 to IL-39. Each class name states its original defining function, which is why the biological-activity table can largely be reconstructed from the class names.
TMU Lecture 5 (Juan Li) Slides 20–24→ read the unitUnit 6 · CDs and CAMs
35CD is short for ? of ? , so named because these molecules appear or disappear at different stages of cell ? and ? .4 mark(s)
The name records the observation, not the function — which is why a CD panel reports both a cell's lineage and its developmental stage.
TMU Lecture 6 — CDs and CAMs Slide 4→ read the unit36The four families of cell adhesion molecules are ? , ? , ? and ? .4 mark(s)
Learn them in this order — it is nearly the order in which they are used during leukocyte extravasation: selectin binds mucin to start rolling, then integrin binds Ig-superfamily CAM for firm adhesion.
TMU Lecture 6 — CDs and CAMs Slide 8→ read the unit37L-selectin is expressed on ? , E-selectin on ? , and P-selectin on ? .3 mark(s)
The initial letters carry the answer. P-selectin is additionally stored preformed in endothelial Weibel–Palade bodies, so it appears on the surface within minutes of TNF-α activation.
TMU Lecture 6 — CDs and CAMs Slide 9→ read the unit38Integrins are heterodimers composed of an ? chain and a ? chain, and mediate ? adhesion.3 mark(s)
Contrast selectins, whose carbohydrate binding is deliberately weak and transient so that the cell rolls rather than being torn away by the flow.
TMU Lecture 6 — CDs and CAMs Slide 12→ read the unit39The three general functions of CAMs are acting as ? and ? in the immune response, mediating leukocyte ? and inflammation, and directing lymphocyte ? .4 mark(s)
Co-receptors are CD4 and CD8; co-stimulators are CD28, CD80 and CD86. Each of the three functions is developed in a later unit.
TMU Lecture 6 — CDs and CAMs Slide 14→ read the unit40The four steps by which a leukocyte leaves a blood vessel are ? , ? of integrins by chemokines, ? adhesion, and ? .4 mark(s)
All four CAM families appear in order: selectin → mucin (rolling), then integrin → Ig superfamily (firm adhesion). The one non-adhesion step is done by a cytokine.
Janeway's Immunobiology 10e §3-19→ read the unitUnit 7 · T Lymphocytes
41T 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 86–87→ read the unit42Positive 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 90–91→ read the unit43In 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 102–103→ read the unit44CD4 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, 107→ read the unit45The 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 109→ read the unit46Positive 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 118→ read the unit47CTLs 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 156–157→ read the unit48Regulatory 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 147–148→ read the unitUnit 8 · B Lymphocytes
49B-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 167→ read the unit50Immature 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 179→ read the unit51The 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 lecture→ read the unit52The 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 168→ read the unit53In 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 178→ read the unit54The 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 184→ read the unit55The 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 199→ read the unitUnit 9 · NK and Innate Cells
56The 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 43→ read the unit57NK 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 45→ read the unit58The 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 28→ read the unit59Macrophages 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 38→ read the unit60Macrophage 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 41→ read the unit61The 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 37→ read the unitUnit 10 · MHC
62In humans the MHC is called the ? complex and is located on chromosome ? ; in mice it is called ? and lies on chromosome ? .4 mark(s)
Phrasing confirmed against the student review sheet and the lecture.
TMU Lecture 10 — MHC Slides 5, 8→ read the unit63The genes coding for class I MHC molecules are ? , ? and ? ; the class II genes are ? , ? and ? .6 mark(s)
Class I genes encode only the α chain; class II genes encode both α and β chains.
TMU Lecture 10 — MHC Slide 7→ read the unit64The peptide-binding cleft of MHC class I is formed by ? and ? ; that of class II by ? and ? .4 mark(s)
This is MCQ Q6. Count the MHC-encoded chains: class I has one, so both groove walls come from it; class II has two, so it takes one domain from each.
Past Papers 2019 & 2020, Section III Q6 · TMU Lecture 10 — MHC Slide 32→ read the unit65MHC class I is expressed on ? cells, whereas class II is expressed only on ? , ? , ? and thymic stromal cells.4 mark(s)
Class I reports (any cell can be infected); class II recruits (only professional APCs may start a response). True/False Q12 swaps the two rules.
TMU Lecture 10 — MHC Slide 15→ read the unit66CD8 binds the ? domain of MHC class I; CD4 binds the ? domain of MHC class II.2 mark(s)
Both are non-polymorphic regions away from the groove, so the co-receptor grip does not depend on which peptide is displayed.
TMU Lecture 10 — MHC Slide 26→ read the unit67MHC class I binds peptides of ? amino acids in a ? cleft; class II binds peptides of ? amino acids in an ? cleft.4 mark(s)
The cleft shape dictates the length rule — a closed cleft grips both termini, an open one lets the peptide overhang.
TMU Lecture 10 — MHC Slide 32→ read the unit68The five properties of MHC are ? , ? , ? , ? and ? .5 mark(s)
Note what is absent: allelic exclusion. Both parental alleles are expressed in every cell.
TMU Lecture 10 — MHC Slide 22→ read the unitUnit 11 · APCs and Processing
69Professional APCs include ? , ? and ? .3 mark(s)
Exactly the cells that express MHC class II constitutively — the professional-APC list and the class II distribution list are the same list.
Past Papers 2019 & 2020, Section II→ read the unit70Endogenous antigen is degraded by the ? , transported to the ER by ? , loaded onto MHC class ? and presented to ? T cells.4 mark(s)
The pathway solves a geography problem: class I is assembled in the ER but its peptides are in the cytosol, so they must be chopped outside and pumped in.
TMU Lecture 8 — Antigen Presenting Cells Slides 18, 22→ read the unit71Exogenous antigen is taken up by ? , degraded in the ? , loaded onto MHC class ? and presented to ? T cells.4 mark(s)
No transporter is needed here — antigen and class II arrive in the same vesicular compartment, so the peptide is simply loaded where they meet.
TMU Lecture 8 — Antigen Presenting Cells Slide 23→ read the unit72An immature DC has antigen uptake ? and antigen presentation ? ; a mature DC has uptake ? and presentation ? .4 mark(s)
This reversal is MCQ Q14. The immature DC collects in peripheral tissue; the mature DC reports in the lymph node.
TMU Lecture 8 — Antigen Presenting Cells Slide 11→ read the unit73Dendritic cells are classified by derivation into ? DC (DC1) and ? DC (DC2).2 mark(s)
By function they are additionally classified as immature or mature.
TMU Lecture 8 — Antigen Presenting Cells Slide 10→ read the unitUnit 12 · The Immune Response
74The 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 9→ read the unit75The 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 64→ read the unit76Signal 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, 76→ read the unit77Activated 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 58→ read the unit78The 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 60→ read the unit79MHC class ? restriction operates between APCs and CD4⁺ T cells; MHC class ? restriction operates between target cells and CD8⁺ CTLs.2 mark(s)
Unit 13 · Type I Hypersensitivity
80The four components of type I hypersensitivity are ? , the antibody ? , the cells ? and ? , and the ? .5 mark(s)
Eosinophils join in the late-phase reaction and also down-regulate the response.
TMU Lecture 11 — Hypersensitivity Slide 28→ read the unit81The three phases of type I hypersensitivity are the ? phase, the ? phase and the ? phase.3 mark(s)
Sensitization is silent; the second exposure causes the reaction.
TMU Lecture 11 — Hypersensitivity Slide 41→ read the unit82IgE binds ? on mast cells and basophils through its ? and ? domains.3 mark(s)
The Fc binds the receptor while the variable region stays free to catch allergen.
TMU Lecture 11 — Hypersensitivity Slide 35→ read the unit83The preformed mediator is ? ; three newly formed mediators are ? , ? and ? .4 mark(s)
Preformed acts immediately; newly formed drive the late phase.
TMU Lecture 11 — Hypersensitivity Slide 39→ read the unit84Mediators of type I cause ? contraction, ? with increased vascular ? , and ? secretion.4 mark(s)
Three effects; the site of the mast cells decides which disease results.
TMU Lecture 11 — Hypersensitivity Slide 47→ read the unit85A positive skin test shows a ? and ? greater than 5 × 5 mm after ? minutes.3 mark(s)
Thirty minutes marks it as immediate — contrast the tuberculin test at 24–48 hours.
TMU Lecture 11 — Hypersensitivity Slide 55→ read the unitUnit 14 · Type II Hypersensitivity
86Type II hypersensitivity is mediated by antibodies ? and ? against antigen located on the ? .3 mark(s)
The antigen's location on a cell is what makes the damage target-specific — the basis of MCQ Q19.
TMU Type II Hypersensitivity deck (Yu Chunyan) Slides 7–8→ read the unit87The three mechanisms of target-cell destruction in type II are ? , ? and ? .3 mark(s)
All three are ordinary antibody effector functions — the pathology is in the target, not the mechanism.
TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 14→ read the unit88The effector components of type II hypersensitivity are ? , ? and ? .3 mark(s)
This is True/False Q10, and it is true. Contrast type I, where the NK cell plays no part.
Past Papers 2019 & 2020, Section IV Q10→ read the unit89Haemolytic disease of the newborn develops when maternal ? against fetal blood-group antigen crosses the ? and destroys fetal ? .3 mark(s)
Only IgG crosses the placenta — the same mechanism that gives newborns passive immunity destroys their red cells here.
TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 18→ read the unit90HDN is prevented by giving ? to the mother within ? hours of the first delivery, which prevents ? activation and ? generation.4 mark(s)
No memory means no secondary response, so no IgG in the next pregnancy.
Past Papers 2019 & 2020, Section IV Q7→ read the unitUnit 15 · Hypersensitivity III & IV
91Immune-complex disease is caused by ? -sized complexes, which are too ? to be phagocytosed and too ? to be filtered by the glomerulus.3 mark(s)
Large complexes are cleared fast by phagocytes; small ones pass into the urine and do not fix complement. Only the middle size is trapped where it can do harm.
TMU Type III & IV Hypersensitivity deck Slide 4→ read the unit92Immune complexes characteristically deposit in the ? of joints, the ? of the kidney, and the ? of the brain.3 mark(s)
All three filter blood under pressure through small vessels.
TMU Type III & IV Hypersensitivity deck Slide 3→ read the unit93In type III hypersensitivity, ? , ? and ? act as chemotactic factors recruiting neutrophils.3 mark(s)
The recruited neutrophils then release lytic enzymes, which cause most of the tissue damage.
TMU Type III & IV Hypersensitivity deck Slide 6→ read the unit94The three properties of type IV hypersensitivity are a delay of ? hours, recruitment of ? , and the involvement of no ? and no ? .4 mark(s)
The delay is itself evidence that no antibody is involved — there is no pre-formed effector waiting.
TMU Type III & IV Hypersensitivity deck Slide 20→ read the unit95In type IV hypersensitivity, ? activates macrophages while ? and ? cause local tissue injury.3 mark(s)
All are Th1 cytokines — which is why Th1 drives type IV and Th2 drives type I.
TMU Type III & IV Hypersensitivity deck Slide 24→ read the unit96A positive OT (tuberculin) test shows red induration about ? mm in diameter at ? hours.2 mark(s)
Contrast the type I skin test — wheal and flare >5 × 5 mm at 30 minutes. The timing distinguishes the mechanisms.
TMU Type III & IV Hypersensitivity deck Slide 28→ read the unitUnit 16 · Immunoassay
97 ? agglutination detects antigen, as in ABO blood typing; ? agglutination detects antibody, as in the rheumatoid factor test.2 mark(s)
The chemistry is the same; only the reagent supplied and the target sought are swapped.
TMU Lecture 12 — Immunoassay (Yu Chunyan) Slide 18→ read the unit98In an allergic patient the antibody mainly involved is ? and the cytokine is ? ; both can be measured by ? .3 mark(s)
The lecture poses this as its own question. IL-4 from Th2 drives the class switch to IgE.
TMU Lecture 12 — Immunoassay (Yu Chunyan) Slide 15→ read the unit99The lymphocyte transformation test uses ? stimulation over ? hours; the E-rosette test works because ? is the sheep-erythrocyte receptor.3 mark(s)
Both assays are applications of facts from Units 2 and 7 — mitogens, and the CD2 E receptor.
TMU Lecture 12 — Immunoassay (Yu Chunyan) Slide 11→ read the unit100Immune cells are evaluated by their ? and their ? .2 mark(s)
A normal count can conceal defective function — which is why a negative tuberculin test may mean immunodeficiency rather than no exposure.
TMU Lecture 12 — Immunoassay (Yu Chunyan) Slide 10→ read the unit101The final goals of immunoassay are ? , ? , ? and ? .4 mark(s)
Immunoassay measures; immunotherapy treats.
TMU Lecture 12 — Immunoassay (Yu Chunyan) Slide 15→ read the unitUnit 17 · Immunotherapy
102Immunotherapy is the treatment of disease with agents that ? or ? the immune response.2 mark(s)
Both directions count — anti-lymphocyte serum for graft rejection is immunotherapy just as much as a vaccine is.
Past Papers 2019 & 2020, Section I→ read the unit103 ? immunotherapy gives antigen, whereas ? or ? immunotherapy gives immune response products.3 mark(s)
Unit 1's active/passive distinction, applied therapeutically.
TMU Lecture 13 — Immunotherapy (Yu Chunyan) Slide 4→ read the unit104A toxoid is an exotoxin treated with ? so that it loses its ? properties but retains its ability to stimulate an ? against the toxin.3 mark(s)
The exam statement in True/False Q8 is this definition, word for word.
Past Papers 2019 & 2020, Section IV Q8→ read the unit105The four features of an effective vaccine are ? , ? , ? and ? .4 mark(s)
106The four types of engineered monoclonal antibody are ? , ? , ? and ? .4 mark(s)
Each step down the list removes more mouse protein while preserving the binding site — which is why drug names end in -ximab (chimeric) or -zumab (humanized).
TMU Lecture 13 — Immunotherapy (Yu Chunyan) Slide 22→ read the unit107The main immune checkpoint molecules targeted therapeutically are ? , ? and ? .3 mark(s)
These are Unit 7's brakes; blocking them releases T-cell activity against tumours.
TMU Lecture 13 — Immunotherapy (Yu Chunyan) Slide 23→ read the unit