Chapter 26 — Quiz

Twenty-two items. Answer key at the end. Several items have a deliberately attractive wrong option; if you are drawn to it, read the explanation rather than just noting the letter.


1. What does a T-cell receptor actually contact?

A. An intact folded protein on a pathogen's surface B. A short peptide held in the groove of an MHC/HLA molecule C. A carbohydrate on a bacterial cell wall D. A free-floating antigen in serum

2. Class I HLA molecules present peptides derived from:

A. Material engulfed from outside the cell B. Proteins made inside the cell C. Only viral proteins D. Only mutated proteins

3. Which cell type recognizes peptides presented on class II?

A. CD8 cytotoxic T cells B. CD4 helper T cells C. Natural killer cells D. Plasma cells

4. Most antibody epitopes on natural proteins are:

A. Linear B. Conformational C. Carbohydrate D. Identical to T-cell epitopes

5. The main reason short peptides make poor prophylactic vaccines against most pathogens is:

A. They are too expensive to manufacture B. They cannot be stored C. Protection usually depends on antibodies, which read conformational surfaces that a short peptide presents poorly D. They are destroyed by the proteasome

6. "HLA restriction" means:

A. Some people cannot mount immune responses at all B. A T cell recognizes its peptide only in the context of a particular HLA molecule C. HLA molecules restrict how much antigen can enter a cell D. Vaccines must be refrigerated

7. The HLA genes are notable because they are:

A. Present only in humans B. Identical in all members of a species C. The most polymorphic genes in the human genome D. Not inherited

8. A peptide vaccine produces a robust response in one person and nothing detectable in another. The explanation this chapter emphasizes most is:

A. The second person's immune system is weaker B. The second person's HLA molecules may not present that peptide at all C. The second person received a lower dose D. The peptide degraded before injection

9. Why is an adjuvant usually essential for a peptide vaccine?

A. It keeps the peptide from dissolving B. It supplies the innate danger signal without which antigen exposure tends to produce anergy or tolerance rather than immunity C. It increases the peptide's molecular weight above the protein threshold D. It prevents anaphylaxis

10. A T cell that encounters its peptide without costimulation typically:

A. Becomes a long-lived memory cell B. Becomes anergic, is deleted, or becomes regulatory C. Kills the presenting cell D. Switches to making antibodies

11. A neoantigen is:

A. Any protein overexpressed by a tumor B. A peptide containing an amino acid change from a somatic mutation, absent from the normal proteome C. A synthetic peptide designed by an algorithm D. Any antigen not previously described in the literature

12. The key immunological advantage of neoantigens over tumor-associated antigens is:

A. They are easier to synthesize B. They are present in more patients C. They are not subject to central tolerance, so the high-affinity repertoire against them is intact D. They do not require HLA presentation

13. In the individualized vaccine pipeline, sequencing normal tissue is required in order to:

A. Confirm the patient's identity B. Establish which sequence changes are somatic rather than inherited C. Measure immune function D. Determine the dose

14. Synthetic long peptides (roughly 20–30 residues) are preferred over minimal 8–10-residue epitopes largely because:

A. They are cheaper B. They bind HLA more tightly C. They must be processed by professional presenting cells, avoiding tolerizing direct loading onto cells that cannot costimulate D. They last longer in circulation

15. An mRNA cancer vaccine is best described as:

A. A peptide drug B. Not a peptide drug, but a peptide-antigen vaccine — the message is still a peptide sequence C. A gene therapy that permanently alters the genome D. A small-molecule immunostimulant

16. The main practical reason individualized programs reached for mRNA rather than peptides is:

A. mRNA is more immunogenic in every case B. One construct encoding many epitopes requires one synthesis, which is far more standardizable than manufacturing many individual peptides per patient C. mRNA does not require an adjuvant of any kind D. Peptides cannot encode more than one epitope

17. As of 2026, the status of individualized neoantigen cancer vaccines is:

A. Approved for general use in melanoma B. Abandoned after phase 3 failures C. In randomized trials, with encouraging early results supporting larger confirmatory trials, and no general approval anywhere D. Available by prescription in most countries

18. The attribution problem in current cancer vaccine trials arises because:

A. Patients are not told which arm they are in B. The vaccines are given alongside checkpoint inhibitors, which are themselves effective C. Recurrence cannot be measured D. Neoantigens cannot be verified

19. In a small single-arm study, patients who mounted a vaccine-induced T-cell response remained recurrence-free longer than those who did not. The correct reading is:

A. The vaccine works B. The vaccine works in immune-competent patients only C. This is a responder-versus-non-responder comparison, not a randomized one, and it motivates a randomized trial rather than establishing benefit D. The vaccine has been disproven

20. The most successful "cancer vaccines" currently in existence are:

A. Therapeutic peptide vaccines in melanoma B. Prophylactic antiviral vaccines against hepatitis B and human papillomavirus C. Autologous cellular immunotherapies D. Oncolytic viruses

21. Peptide-based allergy immunotherapy aims to:

A. Provoke a strong cytotoxic response against the allergen B. Induce tolerance using peptides too small to cross-link IgE and trigger mast cells C. Replace antihistamines D. Remove IgE from circulation

22. This chapter rates individualized neoantigen cancer vaccines 🔬 rather than ⚠️ principally because:

A. The mechanism is unproven B. There is no human data of any kind C. The randomized evidence is early and narrow, the intervention is a manufacturing process rather than a fixed molecule, and no confirmatory trial has established durable benefit D. The approach is implausible


Answer key **1 — B.** A T-cell receptor engages a peptide in an MHC/HLA groove. It cannot see free antigen, whole pathogens, or anything not presented. This is the central mechanical fact of the chapter (§26.2). **2 — B.** Class I samples the cell's internal protein production, which is how a cytotoxic T cell can detect what is happening inside a cell it cannot enter (§26.2). It is not restricted to viral or mutated proteins — it displays normal self peptides constantly, which is exactly why an abnormal one stands out. **3 — B.** Class II presents to CD4 helper T cells, whose help is required for durable CD8 memory and high-quality antibody responses (§26.2). **4 — B.** Antibodies bind three-dimensional surface patches assembled by folding. Unfold the protein and the epitope is gone (§26.2). **5 — C.** The reason is structural, not logistical. Peptide immunogens routinely raise antibodies that bind the peptide well and the folded pathogen badly (§26.2, §26.7). **6 — B.** The recognition event is peptide *plus* HLA, not peptide alone (§26.3). **7 — C.** Tens of thousands of alleles have been cataloged, with much of the variation concentrated in the peptide-binding groove (§26.3). **8 — B.** Option A is the intuitive answer and is usually wrong. Non-presentation is not a weak response; it is a mechanism that never engaged (§26.3). **9 — B.** Foreignness alone does not provoke immunity — foreignness plus danger does. Without the danger signal, you may induce tolerance instead (§26.4). **10 — B.** This is the mechanism by which vaccination can make things worse, and it is one plausible explanation for historical trials in which vaccinated patients did no better or slightly worse (§26.4). **11 — B.** The defining feature is absence from the normal proteome. Overexpressed self proteins are tumor-*associated* antigens, a different and much harder category (§26.5). **12 — C.** Tolerance is the deepest problem in therapeutic cancer vaccination, and neoantigens are the one antigen class that sidesteps it rather than fighting it (§26.5). **13 — B.** Without a matched normal sample you cannot tell a somatic mutation from an inherited variant, and inherited variants are self — tolerized, and potentially dangerous to target (§26.5). **14 — C.** Minimal epitopes load directly onto class I on any cell, including cells that cannot costimulate. That is the tolerizing presentation described in §26.4. Long peptides also carry class II epitopes and recruit CD4 help (§26.5). **15 — B.** Nothing peptide-shaped is administered, so it is not a peptide drug; but the therapeutic message is a peptide sequence, and only the delivery differs (§26.6). Option C is false and worth naming as false. **16 — B.** Twenty individualized peptides means twenty manufacturing processes for one patient; one mRNA construct encoding twenty epitopes is one process, identical in shape no matter what the algorithm chose (§26.6). **17 — C.** State the stage, not results you cannot source. No individualized neoantigen cancer vaccine has general approval as of 2026 (§26.7). **18 — B.** Randomization with the checkpoint inhibitor in both arms solves this in principle; the difficulty is powering and follow-up, not logic (§26.7). **19 — C.** Patients able to mount a strong immune response may differ systematically from those who cannot. This confound has misled oncology repeatedly (§26.7). **20 — B.** They prevent the chronic viral infections that cause the cancers, they are given to healthy people, and neither is a peptide vaccine. They succeeded by solving the easier problem (§26.8). **21 — B.** Cross-linking requires two spatially separated B-cell epitopes on one molecule; a short peptide cannot bridge two IgE molecules. The goal is tolerance, not immunity (§26.9). **22 — C.** Note that A and B are both false — the mechanism is ✅ and randomized human data exist. The rating turns on the narrowness of the randomized evidence, the process-not-molecule problem, and the absence of a completed confirmatory trial (§26.10).