Free MCAT-style practice, 3B
MCAT Immune System Practice Questions
Ten free MCAT-style immune system practice questions on innate defenses, complement, B cells and antibody responses, T cells and MHC, vaccines and hypersensitivity, with full explanations.
Quick concept primer
Innate immunity is fast, nonspecific and has no memory. Barriers such as skin and mucus come first, then neutrophils, macrophages, dendritic cells and natural killer cells, which recognize broad microbial patterns through receptors such as Toll-like receptors. Complement proteins coat microbes for phagocytosis (C3b), recruit cells (C5a) and punch holes in membranes (the C5b to C9 membrane attack complex).
Adaptive immunity is slower the first time, highly specific, and remembers. MHC class I, on nearly all nucleated cells, shows peptides from inside the cell to CD8 cytotoxic T cells, which kill infected or abnormal cells. MHC class II, on antigen-presenting cells, shows peptides from engulfed material to CD4 helper T cells, which direct B cells and macrophages. A naive T cell needs both antigen recognition and a costimulatory signal; without the second signal it becomes unresponsive. B cells selected by antigen become plasma cells and memory cells. IgM dominates a first response, while a second exposure brings a faster, larger IgG response. Vaccines create active immunity with memory; transferred antibodies give passive, short-lived protection.
Traps: CD8 pairs with MHC I and CD4 with MHC II, NK cells attack cells that lack MHC I, and type IV hypersensitivity involves T cells, not antibody.
10 practice questions
Question 1
A respiratory virus infects airway epithelial cells, and viral proteins are made in their cytoplasm. How are infected epithelial cells recognized and killed by the adaptive immune system?
- Viral peptides on MHC class II are recognized by CD4 helper T cells, which lyse the cells
- Viral peptides on MHC class I are recognized by CD8 cytotoxic T cells
- IgE bound to mast cells recognizes the infected cells
- Neutrophils recognize viral peptides on MHC class I
Show answer and explanation
Answer: B. Viral peptides on MHC class I are recognized by CD8 cytotoxic T cells
Proteins made in the cytosol are broken down by proteasomes, and the peptides are loaded onto MHC class I, which almost every nucleated cell displays. CD8 cytotoxic T cells recognize these complexes and kill the cell with perforin and granzymes. Epithelial cells generally lack MHC class II, helper T cells coordinate rather than lyse, and neutrophils do not read MHC peptides.
Question 2
A tumor cell stops expressing MHC class I molecules, which lets it avoid cytotoxic T cells. Which cell is best suited to kill it?
- A natural killer cell
- A CD4 helper T cell
- A plasma cell
- An eosinophil
Show answer and explanation
Answer: A. A natural killer cell
Natural killer cells are inhibited by MHC class I on healthy cells, so a cell that loses MHC class I removes that brake and becomes a target for NK cell killing. This complements cytotoxic T cells, which require MHC class I to recognize a target. Helper T cells recognize MHC class II, plasma cells secrete antibody, and eosinophils mainly fight parasites.
Question 3
Antibody titers (the highest dilution that still gives a positive test) were measured after a first and a second injection of the same antigen given months apart.
| Response | Peak IgM titer | Peak IgG titer |
|---|---|---|
| After first injection | 160 | 80 |
| After second injection | 160 | 2560 |
By what factor did the peak IgG titer increase, and which feature of adaptive immunity explains it?
- 16-fold, because of innate immune training
- 32-fold, because IgM was converted into IgG in the blood
- 2-fold, because the antigen dose was doubled
- 32-fold, because memory B cells that had already switched to IgG responded
Show answer and explanation
Answer: D. 32-fold, because memory B cells that had already switched to IgG responded
The IgG titer rose from 80 to 2560, and 2560 / 80 = 32, a 32-fold increase. During the first response some B cells class-switched and became memory cells; on second exposure they respond faster and produce far more IgG, while IgM changes little. Class switching happens in the B cell's DNA, not by converting antibody molecules already circulating in the blood.
Question 4
Each of the following hypersensitivity reactions is mediated by antibody EXCEPT:
- Anaphylaxis after a bee sting
- Red cell destruction after an ABO-mismatched transfusion
- Contact dermatitis appearing two days after touching nickel jewelry
- Serum sickness from immune complexes deposited in small vessels
Show answer and explanation
Answer: C. Contact dermatitis appearing two days after touching nickel jewelry
Contact dermatitis is a type IV, delayed hypersensitivity reaction driven by sensitized T cells, which is why it takes a day or more to appear and involves no antibody. Anaphylaxis is type I (IgE on mast cells), a transfusion reaction is type II (antibody against cell-surface antigens), and serum sickness is type III (immune complex deposition).
Question 5
A newborn is protected from several infections during the first months of life by maternal antibody that crossed the placenta. Which statement about this protection is correct?
- It is passive immunity provided by IgG and gives the infant no lasting memory
- It is active immunity provided by IgA and lasts for life
- It is passive immunity provided by IgM, the only antibody that crosses the placenta
- It is active immunity because the infant's B cells made the antibody
Show answer and explanation
Answer: A. It is passive immunity provided by IgG and gives the infant no lasting memory
IgG is the only antibody class transported across the placenta, and receiving ready-made antibody is passive immunity. The infant's own B cells were never activated, so no memory forms and protection fades as the maternal IgG is cleared over months. IgA reaches the infant through breast milk, and IgM is too large to cross the placenta.
Question 6
For a vaccine that fully blocks transmission, a common estimate of the fraction of a population that must be immune to stop sustained spread is 1 minus 1/R0, where R0 is the average number of people one case infects in a fully susceptible population. What fraction is needed for a disease with an R0 of 4?
- 25 percent
- 40 percent
- 75 percent
- 96 percent
Show answer and explanation
Answer: C. 75 percent
Using the given expression, 1 minus 1/4 = 0.75, so about 75 percent of the population must be immune. Then each case infects fewer than one new person on average, and outbreaks die out. The 25 percent figure is 1/R0 itself, and the larger values do not follow from the formula. A higher R0 always raises the threshold.
Question 7
During T cell development in the thymus, what happens to a developing T cell whose receptor binds very strongly to a self-peptide presented on self-MHC?
- It is deleted by apoptosis during negative selection
- It is kept because strong binding shows it can recognize self-MHC
- It matures into a plasma cell
- It leaves the thymus as a naive cytotoxic T cell
Show answer and explanation
Answer: A. It is deleted by apoptosis during negative selection
Negative selection removes T cells whose receptors bind self-peptide and MHC too strongly, because they could attack the body's own tissues; this is central tolerance. Positive selection keeps cells that bind self-MHC weakly enough to be useful. Plasma cells develop from B cells, and releasing strongly self-reactive cells would promote autoimmunity.
Question 8
A patient's complement components C5 through C9 cannot assemble. Which complement function is lost?
- Coating bacteria with C3b to promote phagocytosis
- Formation of membrane pores that lyse bacteria
- Activation of the classical pathway by antibody
- Recognition of bacteria by Toll-like receptors
Show answer and explanation
Answer: B. Formation of membrane pores that lyse bacteria
C5b through C9 assemble into the membrane attack complex, a pore that lets water and ions rush into thin-walled bacteria such as Neisseria species and lyses them. Opsonization by C3b and classical pathway activation happen upstream and would still work. Toll-like receptors are separate pattern recognition receptors, not complement proteins.
Question 9
Which feature distinguishes the innate immune response from the adaptive immune response?
- Innate responses rely on receptors produced by gene rearrangement in each lymphocyte
- Innate responses become faster and stronger with each repeat exposure through memory cells
- Innate responses are generated only after antigen is presented on MHC class II
- Innate responses begin within minutes to hours and use receptors that recognize patterns shared by many microbes
Show answer and explanation
Answer: D. Innate responses begin within minutes to hours and use receptors that recognize patterns shared by many microbes
Innate defenses are ready before infection and use germline-encoded pattern recognition receptors, such as Toll-like receptors binding lipopolysaccharide, to respond within minutes to hours. Gene rearrangement of receptors, memory that strengthens repeat responses, and dependence on antigen presentation to helper T cells are hallmarks of adaptive immunity.
Question 10
A drug blocks binding between B7 on antigen-presenting cells and CD28 on T cells. What is the most likely effect on a naive T cell that recognizes its antigen while the drug is present?
- It becomes a memory T cell immediately
- It becomes anergic and fails to proliferate
- It differentiates into a B cell
- It kills the antigen-presenting cell
Show answer and explanation
Answer: B. It becomes anergic and fails to proliferate
Activating a naive T cell takes two signals: the T cell receptor binding peptide on MHC, and costimulation through CD28 binding B7. Antigen recognition without costimulation leaves the cell anergic, unresponsive to later stimulation, which is a form of peripheral tolerance. The cell does not proliferate, so it cannot form memory or effector cells, and T cells never become B cells.