BT302 — Immunology | VU Solved MCQs

BT302 Immunology covers Lymphoid organs, Innate immunity, B cells, Cytokines, T helper cell subsets, Antigenic variation, Complement system, Cells of the immune system, Antigen presentation, Hypersensitivity, Vaccines, Monoclonal antibodies, Immunological techniques, Autoimmunity, Innate vs adaptive immunity and Antibody structure. This solved post gives you 30 verified items for Virtual University of Pakistan, 10 Midterm MCQs from Lectures 1-22, 10 Finalterm MCQs from Lectures 23-45, and 5 Midterm plus 5 Finalterm subjective questions, each with its correct answer and handout reference. Practice every question instantly in the quiz for this course. Take the BT302 quiz

1. Midterm Solved MCQs

Q1. Which two organs are the primary lymphoid organs, in which immunocompetent cells originate and mature?
A) Thyroid and Peyer's patches
B) Thymus and bone marrow
C) Spleen and mucosal-associated lymphoid tissue (MALT)
D) Lymph nodes and thoracic duct
Correct answer: B — Thymus and bone marrow
Reference: VU handout — Lymphoid organs; primary vs secondary lymphoid organs.
Status: Verified

Q2. Which of the following is an example of innate immunity?
A) Antibody production by plasma cells
B) Antigen removal by cilia in the respiratory tract
C) Complement activation by antibody bound to a bacterium
D) Memory response to influenza virus
Correct answer: B — Antigen removal by cilia in the respiratory tract
Reference: VU handout — Innate immunity; physical barriers.
Status: Verified

Q3. Plasma cells produce thousands of __________ that are released into the bloodstream.
A) Antigens
B) Antibodies
C) Helper T cells
D) Virus fragments
Correct answer: B — Antibodies
Reference: VU handout — B cells; plasma cells.
Status: Verified

Q4. Which cytokine is involved in the class switching of antibody to IgE?
A) TGF-β
B) IL-5
C) IL-2
D) IL-4
Correct answer: D — IL-4
Reference: VU handout — Cytokines; antibody class switching.
Status: Verified

Q5. Th2 cells upon activation secrete cytokines like IL-4 and IL-5 which activate __________.
A) Antigen-presenting cells (APC)
B) Cytotoxic T lymphocytes (CTL)
C) Macrophages
D) B-cells
Correct answer: D — B-cells
Reference: VU handout — T helper cell subsets; Th2 response.
Status: Verified

Q6. A major form of change in antigenic structure that results in new strains of a microbe is called:
A) Antigenic shift
B) Antigenic drift
C) Antigenic variation
D) Antigenic mutation
Correct answer: A — Antigenic shift
Reference: VU handout — Antigenic variation; influenza.
Status: Verified

Q7. Chemokines are cytokines responsible for:
A) Leucocyte proliferation
B) Leucocyte migration
C) Leucocyte inhibition
D) Leucocyte killing
Correct answer: B — Leucocyte migration
Reference: VU handout — Cytokines; chemokines.
Status: Verified

Q8. Which complement component is found in both the classical and the alternative pathways?
A) C1
B) C2
C) Factor D
D) C3
Correct answer: D — C3
Reference: VU handout — Complement system.
Status: Verified

Q9. Which immunoglobulin(s) help initiate the classical complement pathway?
A) IgA and IgD
B) IgM only
C) IgG and IgM
D) IgG only
Correct answer: C — IgG and IgM
Reference: VU handout — Complement system; classical pathway.
Status: Verified

Q10. Which white blood cells are the most abundant in blood and the first to arrive at a site of acute bacterial infection?
A) Eosinophils
B) Basophils
C) Neutrophils
D) Lymphocytes
Correct answer: C — Neutrophils
Reference: VU handout — Cells of the immune system; phagocytes.
Status: Verified

2. Finalterm Solved MCQs

Q1. Antigen presented on MHC class I molecules is recognised by:
A) CD4+ helper T cells
B) CD8+ cytotoxic T cells
C) B cells directly
D) Natural killer cells only
Correct answer: B — CD8+ cytotoxic T cells
Reference: VU handout — Antigen presentation; MHC class I.
Status: Verified

Q2. Antigen presented on MHC class II molecules is recognised by:
A) CD8+ cytotoxic T cells
B) CD4+ helper T cells
C) Plasma cells
D) Mast cells
Correct answer: B — CD4+ helper T cells
Reference: VU handout — Antigen presentation; MHC class II.
Status: Verified

Q3. Type I hypersensitivity (immediate, anaphylactic) is mediated mainly by:
A) IgG and complement
B) IgE and mast cells
C) Immune complexes
D) T cells
Correct answer: B — IgE and mast cells
Reference: VU handout — Hypersensitivity; Type I.
Status: Verified

Q4. A haemolytic transfusion reaction, in which antibody binds to antigens on red blood cells and causes their destruction, is an example of:
A) Type I hypersensitivity
B) Type II hypersensitivity
C) Type III hypersensitivity
D) Type IV hypersensitivity
Correct answer: B — Type II hypersensitivity
Reference: VU handout — Hypersensitivity; Type II.
Status: Verified

Q5. Type IV hypersensitivity differs from Types I–III because it is:
A) Mediated by IgE
B) Mediated by immune complexes
C) Cell-mediated, involving T cells and macrophages, with a delayed onset
D) Caused by complement deficiency
Correct answer: C — Cell-mediated, involving T cells and macrophages, with a delayed onset
Reference: VU handout — Hypersensitivity; Type IV (delayed-type).
Status: Verified

Q6. Immunisation by vaccination gives:
A) Passive natural immunity
B) Passive artificial immunity
C) Active artificial immunity
D) No immunological memory
Correct answer: C — Active artificial immunity
Reference: VU handout — Immunity; active vs passive.
Status: Verified

Q7. Which type of vaccine generally gives the longest-lasting immunity with a single dose, but is unsafe in immunocompromised people?
A) Killed (inactivated) vaccine
B) Live attenuated vaccine
C) Toxoid vaccine
D) Subunit vaccine
Correct answer: B — Live attenuated vaccine
Reference: VU handout — Vaccines; types of vaccines.
Status: Verified

Q8. In a pregnancy test based on monoclonal antibodies, the antibodies detect:
A) Insulin in the blood
B) Human chorionic gonadotropin (hCG) in urine or blood
C) Haemoglobin in urine
D) Thyroxine in saliva
Correct answer: B — Human chorionic gonadotropin (hCG) in urine or blood
Reference: VU handout — Monoclonal antibodies; hybridoma technology.
Status: Verified

Q9. The ELISA test is used to detect:
A) Only bacterial DNA
B) Specific antigens or antibodies in a sample
C) Chromosome number
D) Blood glucose level
Correct answer: B — Specific antigens or antibodies in a sample
Reference: VU handout — Immunological techniques; ELISA.
Status: Verified

Q10. Rheumatoid arthritis and type 1 diabetes mellitus are examples of:
A) Immunodeficiency diseases
B) Autoimmune diseases
C) Type I hypersensitivity
D) Complement deficiencies
Correct answer: B — Autoimmune diseases
Reference: VU handout — Autoimmunity.
Status: Verified

3. Midterm Subjective

Q1. Differentiate between innate and adaptive immunity.
Answer: Innate immunity is present from birth, acts immediately (minutes to hours), is non-specific (the same response to any pathogen), has no memory, and its components are physical barriers (skin, mucosa, cilia), phagocytes (neutrophils, macrophages), NK cells, complement and inflammation. Adaptive immunity develops after exposure, takes days to become effective, is specific (each lymphocyte receptor recognises one antigen), has memory (faster, stronger secondary response), and its components are B cells/antibodies (humoral immunity) and T cells (cell-mediated immunity). Innate immunity is the first line and also activates adaptive immunity; adaptive immunity is needed to clear infections that innate defences cannot control.
Reference: VU handout — Innate vs adaptive immunity.
Status: Verified

Q2. Describe the structure of an IgG antibody molecule and the functions of its Fab and Fc regions.
Answer: IgG is a Y-shaped molecule of about 150 kDa made of four polypeptide chains: two identical heavy chains and two identical light chains, held together by disulphide bonds. Each chain has a variable region (VH or VL) at the N-terminus and constant regions (CH1–CH3, CL). The two antigen-binding sites are formed by the paired VH and VL domains at the tips of the arms. The Fab region (fragment, antigen-binding) is the arms of the Y: it binds the antigen specifically. The Fc region (fragment, crystallisable) is the stem: it binds Fc receptors on phagocytes and NK cells and binds C1q to activate complement, so it links antigen recognition to effector functions such as phagocytosis, antibody-dependent cellular cytotoxicity (ADCC) and complement activation. IgG is the most abundant antibody in blood, crosses the placenta, and is the main antibody of the secondary response.
Reference: VU handout — Antibody structure; immunoglobulin classes.
Status: Verified

Q3. Distinguish primary from secondary lymphoid organs, giving two examples of each and their functions.
Answer: Primary lymphoid organs are where lymphocytes are produced and mature: the bone marrow (B cells mature here; it is the source of all haematopoietic cells) and the thymus (T cells mature here, undergoing positive and negative selection). Secondary lymphoid organs are where mature lymphocytes meet antigen and are activated: the spleen (filters blood-borne antigens), lymph nodes (filter lymph and drain tissues), and mucosa-associated lymphoid tissue such as Peyer's patches (guard mucosal surfaces). Lymphocytes recirculate between blood and secondary organs, so an antigen entering anywhere in the body is likely to meet a lymphocyte that can recognise it.
Reference: VU handout — Lymphoid organs.
Status: Verified

Q4. What is the complement system? Name its three activation pathways and its main biological functions.
Answer: The complement system is a set of about 30 plasma and cell-surface proteins that act in a cascade to destroy pathogens and promote inflammation. It is activated by three pathways, all converging on C3: (1) the classical pathway, triggered when C1q binds antibody (IgG or IgM) attached to antigen; (2) the lectin pathway, triggered when mannose-binding lectin binds microbial sugars; (3) the alternative pathway, triggered directly by microbial surfaces (spontaneous C3 hydrolysis). Its main functions are: opsonisation (C3b coats microbes so phagocytes ingest them), inflammation (C3a and C5a recruit and activate leukocytes), and direct killing (the membrane attack complex C5b–C9 forms pores in bacterial membranes). Complement activity is destroyed by heating serum at 56 °C for 30 minutes.
Reference: VU handout — Complement system.
Status: Verified

Q5. Explain antigen processing and presentation. How do the MHC class I and class II pathways differ?
Answer: T cells cannot see free antigen; they recognise short peptides bound to MHC molecules on a cell surface. In the MHC class I pathway, proteins made inside the cell (e.g. viral proteins) are degraded by the proteasome, the peptides are transported into the endoplasmic reticulum by TAP, loaded onto MHC class I molecules, and displayed to CD8+ cytotoxic T cells, which then kill the infected cell. In the MHC class II pathway, proteins taken up from outside the cell are degraded in endosomes/lysosomes, loaded onto MHC class II molecules, and displayed to CD4+ helper T cells, which then activate B cells and macrophages. In short: class I presents endogenous (intracellular) antigen to CD8 cells; class II presents exogenous (extracellular) antigen to CD4 cells. Professional antigen-presenting cells (dendritic cells, macrophages, B cells) express MHC class II; almost all nucleated cells express MHC class I.
Reference: VU handout — Antigen processing and presentation; MHC.
Status: Verified

4. Finalterm Subjective

Q1. Describe the four types of hypersensitivity (Gell and Coombs classification), giving the mechanism and one example of each.
Answer: Type I — immediate/anaphylactic: IgE on mast cells; on re-exposure the allergen cross-links IgE, mast cells degranulate (histamine), causing allergy, asthma or anaphylaxis within minutes. Type II — antibody-mediated cytotoxic: IgG/IgM binds antigens on cell surfaces and destroys the cells via complement or phagocytes, e.g. haemolytic transfusion reaction, haemolytic disease of the newborn. Type III — immune-complex: soluble antigen–antibody complexes deposit in tissues (joints, kidney, vessel walls), activate complement and cause inflammation, e.g. serum sickness, systemic lupus erythematosus. Type IV — delayed-type, cell-mediated: CD4 Th1 cells and macrophages respond 48–72 hours later without antibody, e.g. the tuberculin skin test, contact dermatitis. Types I–III are antibody-mediated; Type IV is T-cell mediated.
Reference: VU handout — Hypersensitivity.
Status: Verified

Q2. Distinguish active from passive immunisation, with examples. Why does vaccination produce long-lasting protection?
Answer: Active immunisation is giving antigen (a vaccine) so the person's own immune system responds: it produces antibodies and memory B and T cells, giving long-lasting (often lifelong) protection, but it takes days to weeks to develop. Examples: measles, polio, hepatitis B vaccines. Passive immunisation is giving ready-made antibody (or immune cells) from another person or animal: protection is immediate but temporary (weeks to months) because no memory is formed and the antibody is cleared. Examples: maternal IgG crossing the placenta, antitoxin/antivenom serum, immunoglobulin for hepatitis A. Vaccination lasts because memory lymphocytes persist for years and respond rapidly and strongly on re-exposure (secondary response), and live vaccines in particular mimic natural infection.
Reference: VU handout — Immunity; immunisation.
Status: Verified

Q3. What are monoclonal antibodies? Describe hybridoma technology and give three medical uses.
Answer: A monoclonal antibody is a single antibody specificity produced by one clone of B cells (and their descendants), unlike the mixture of antibodies in serum. Hybridoma technology (Köhler and Milstein, 1975): an animal is immunised with the antigen; its spleen B cells (which make the wanted antibody but die in culture) are fused with myeloma cells (immortal but making no antibody); the fused hybridoma cells are selected (HAT medium) and cloned, giving an immortal cell line secreting one antibody in unlimited amounts. Uses: (1) diagnostics — pregnancy tests (anti-hCG), ELISA and blood grouping; (2) therapy — anti-cancer antibodies (e.g. trastuzumab against HER2, rituximab against CD20), anti-TNF antibodies in rheumatoid arthritis; (3) research and purification — detecting specific proteins, immunoaffinity purification.
Reference: VU handout — Monoclonal antibodies.
Status: Verified

Q4. Classify vaccines and explain each type with an example, including recombinant vaccines.
Answer: (1) Live attenuated vaccines: weakened microbes that replicate briefly and mimic natural infection, giving strong, long-lasting immunity (BCG, measles, oral polio); not for immunocompromised people. (2) Killed/inactivated vaccines: microbes killed by heat or chemicals, safe but usually need boosters (inactivated polio, rabies). (3) Subunit vaccines: only a purified part of the microbe, e.g. a protein or polysaccharide (hepatitis B surface antigen, acellular pertussis). (4) Toxoid vaccines: inactivated toxins (tetanus and diphtheria toxoids). (5) Recombinant/DNA vaccines: the antigen gene is cloned and expressed in yeast or another host (recombinant hepatitis B vaccine produced in yeast) or delivered as DNA; these are third-generation vaccines, safe and precisely defined, with no risk of the disease itself. Modern additions include mRNA vaccines, which deliver mRNA encoding the antigen.
Reference: VU handout — Vaccines.
Status: Verified

Q5. What is autoimmunity? Explain how self-tolerance breaks down and give examples of autoimmune diseases.
Answer: Autoimmunity is an immune response against the body's own (self) antigens. Normally self-tolerance prevents this: self-reactive lymphocytes are deleted in the thymus/bone marrow (central tolerance) or silenced in the periphery (anergy, regulatory T cells). Tolerance can break down through: molecular mimicry (a microbial antigen resembles a self-antigen, e.g. streptococcal antigens and heart tissue in rheumatic fever); release of sequestered antigens (e.g. after eye or testis injury); failure of regulatory T cells; genetic predisposition (certain HLA types); and polyclonal B-cell activation by infection. Examples: type 1 diabetes (immune destruction of pancreatic beta cells), rheumatoid arthritis (joints), systemic lupus erythematosus (many tissues, anti-nuclear antibodies), multiple sclerosis (myelin), Hashimoto's thyroiditis. Treatment aims to suppress the harmful response (immunosuppressive drugs) while preserving defence against infection.
Reference: VU handout — Autoimmunity; tolerance.
Status: Verified

Frequently asked questions

Is the Midterm from Lectures 1-22?
Yes — Midterm covers Lectures 1-22 and Finalterm covers Lectures 23-45.

Does the quiz work from this post?
Yes — use the 'Take the BT302 quiz' link above; the quiz is already live for this course.

Are the answers verified?
Yes — all 30 items are marked Verified, solved independently and cross-checked against at least two independent sources.

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