Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 861: Which of the following immunoglobulins shows homocytotropism?

A. IgG
B. IgA
C. IgE (Correct Answer)
D. IgD

Explanation: ### Explanation **Correct Answer: C. IgE** **Concept of Homocytotropism:** Homocytotropism refers to the unique property of an antibody to bind specifically to the surface of cells (primarily mast cells and basophils) of the same species. This binding occurs via the **Fc region** of the antibody to high-affinity **FcεRI receptors** on the target cells. **IgE** is the classic homocytotropic antibody. When an allergen cross-links these cell-bound IgE molecules, it triggers degranulation and the release of pharmacological mediators like histamine, leading to Type I Hypersensitivity reactions. **Analysis of Incorrect Options:** * **IgG (Option A):** While IgG is the most abundant antibody and can cross the placenta, it is generally not homocytotropic. Some subclasses (like IgG4) may show weak binding, but IgE is the definitive answer for this property. * **IgA (Option B):** Known as the "secretory antibody," its primary role is mucosal immunity. It exists as a dimer in secretions and does not bind to mast cells to mediate anaphylaxis. * **IgD (Option D):** Primarily acts as a B-cell surface receptor. Its precise systemic function is less defined, and it does not exhibit homocytotropic properties. **High-Yield NEET-PG Pearls:** * **Prausnitz-Küstner (PK) Reaction:** A classic historical test used to demonstrate homocytotropism by injecting serum from an allergic individual into the skin of a non-allergic person. * **Heat Lability:** IgE is the most heat-labile immunoglobulin (inactivated at 56°C for 30–60 minutes). * **Reaginic Antibody:** IgE is also known as the reagin antibody. * **Parasitic Infections:** IgE levels are characteristically elevated in helminthic infections and Type I hypersensitivity (Atopy).

Question 862: A latent, measles-like viral infection and, presumably, a defect in cellular immunity is associated with which of the following diseases?

A. Progressive multifocal leukoencephalopathy (PML)
B. Multiple sclerosis (MS)
C. Creutzfeldt-Jakob disease
D. Subacute sclerosing panencephalitis (SSPE) (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Subacute sclerosing panencephalitis (SSPE)** **Subacute sclerosing panencephalitis (SSPE)** is a progressive, fatal demyelinating disease of the central nervous system. It is caused by a **persistent (latent) infection** with a mutant strain of the **Measles virus** (Rubeola). * **Pathogenesis:** The virus involved is a defective variant that lacks the **M (Matrix) protein**, preventing the virus from budding and allowing it to spread directly from cell to cell, evading the immune system. * **Immune Defect:** While the patient has high titers of anti-measles antibodies in the serum and CSF (oligoclonal bands), there is a presumed **defect in cellular immunity** (T-cell response) that fails to clear the latent infection. It typically occurs 5–10 years after an initial measles infection in early childhood. **Why other options are incorrect:** * **A. Progressive multifocal leukoencephalopathy (PML):** Caused by the **JC virus** (a polyomavirus). It occurs in severely immunocompromised patients (e.g., AIDS) but is not related to the measles virus. * **B. Multiple sclerosis (MS):** An autoimmune demyelinating disorder. While viral triggers are suspected (like EBV), it is not caused by a latent measles infection. * **C. Creutzfeldt-Jakob disease:** A neurodegenerative condition caused by **Prions** (infectious proteins), not viruses. It presents with rapidly progressive dementia and myoclonus. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Characterized by **high titers of measles antibodies** in the CSF and **Periodic Synchronous Discharges** on EEG. * **Histology:** Presence of **Cowdry Type A** intranuclear inclusion bodies in neurons and glial cells. * **Clinical Stages:** Progresses from behavioral changes to myoclonus, and eventually to akinetic mutism. * **Prevention:** The most effective way to prevent SSPE is through **Measles vaccination (MMR)**.

Question 863: Which of the following streptococcal antigens cross-reacts with synovial fluid?

A. Carbohydrate (group A)
B. Cell wall protein
C. Capsular hyaluronic acid (Correct Answer)
D. Peptidoglycan

Explanation: ### Explanation The correct answer is **C. Capsular hyaluronic acid**. **Mechanism of Cross-reactivity:** *Streptococcus pyogenes* (Group A Streptococcus) possesses a capsule composed of **hyaluronic acid**. This polysaccharide is chemically identical to the hyaluronic acid found in human connective tissues, particularly in **synovial fluid** and joint cartilage. Because the body recognizes hyaluronic acid as "self," the capsule is non-immunogenic (it does not elicit an immune response), allowing the bacteria to evade phagocytosis. However, in the context of post-streptococcal sequelae like Acute Rheumatic Fever, this molecular mimicry is a key factor in tissue targeting. **Analysis of Incorrect Options:** * **A. Carbohydrate (Group A):** This is the C-substance used for Lancefield grouping. It cross-reacts specifically with the **cardiac valves** (specifically bovine heart valves and human glycoprotein). * **B. Cell wall protein (M-protein):** This is the major virulence factor. It cross-reacts with **cardiac myosin** and sarcolemmal membrane proteins, leading to rheumatic carditis. * **D. Peptidoglycan:** While it provides structural integrity and has some pyrogenic properties, it is not the primary antigen associated with synovial cross-reactivity. **NEET-PG High-Yield Pearls:** * **Molecular Mimicry Table:** * **Capsule:** Synovial fluid/Joints. * **M-Protein:** Myocardium (Myosin). * **Group A Carbohydrate:** Cardiac valves. * **Cytoplasmic Membrane:** Subthalamic/Caudate nuclei (linked to Sydenham’s Cholera). * **Protoplast membrane** is also a significant cross-reactive antigen with the sarcolemma of the heart. * **Key Concept:** The hyaluronic acid capsule is the reason why *S. pyogenes* is often described as "a wolf in sheep's clothing."

Question 864: All of the following are TRUE about ASO titre, EXCEPT?

A. ASO titre can be increased in school children.
B. ASO titre may be negative in post-streptococcal glomerulonephritis.
C. ASO titre is included in the major criteria of the Jones criteria. (Correct Answer)
D. ASO titre may not be elevated in 20% of cases of carditis.

Explanation: **Explanation:** The **Antistreptolysin O (ASO) titre** is a serological marker used to detect a recent infection with Group A Streptococcus (GAS). **1. Why Option C is the Correct Answer (The False Statement):** According to the **Revised Jones Criteria** for the diagnosis of Acute Rheumatic Fever (ARF), the ASO titre is categorized as **evidence of a preceding streptococcal infection**, not as a Major criterion. The Major criteria (mnemonic: **JONES**) include Joint (Polyarthritis), Carditis, Nodules, Erythema marginatum, and Sydenham’s chorea. Evidence of infection (elevated ASO or positive throat culture) is a mandatory requirement for diagnosis alongside the Jones criteria. **2. Analysis of Other Options:** * **Option A:** School-aged children (5–15 years) are the primary demographic for streptococcal pharyngitis; thus, baseline ASO levels are naturally higher in this group compared to adults. * **Option B:** In **Post-Streptococcal Glomerulonephritis (PSGN)** following a skin infection (impetigo), the ASO response is often weak or absent. In such cases, Anti-DNase B is a more reliable marker. * **Option C:** Approximately **20% of ARF cases** (especially those presenting with isolated chorea or late-onset carditis) may show a normal ASO titre because the peak antibody levels have already subsided by the time symptoms appear. **Clinical Pearls for NEET-PG:** * **Peak Timing:** ASO levels peak 3–4 weeks after the initial sore throat. * **Diagnostic Threshold:** A single titre >200 IU/ml is significant in adults, but a **four-fold rise** in paired sera is more diagnostic. * **False Positives:** Liver disease and bacterial contamination of serum can cause false-positive ASO elevations. * **Best Marker for Skin Infections:** Anti-DNase B is superior to ASO for diagnosing PSGN following pyoderma.

Question 865: What is the significance of mutation of CCR5 protein?

A. High resistance to HIV infection (Correct Answer)
B. High susceptibility to HIV infection
C. Causes resistance to anti-retroviral therapy
D. Causes increased virulence of the virus

Explanation: ### Explanation **Core Concept:** HIV-1 primarily enters host CD4+ T-cells by binding to the CD4 receptor and a specific co-receptor. The **CCR5 protein** is a chemokine receptor that serves as the essential co-receptor for **M-tropic (Macrophage-tropic)** strains of HIV, which are responsible for the initial infection and transmission. A specific mutation known as the **CCR5-Δ32 (delta 32) mutation** results in a truncated, non-functional protein that is not expressed on the cell surface. Individuals who are **homozygous** for this mutation lack the "doorway" for the virus to enter, conferring **high resistance to HIV infection**. Heterozygotes typically show a slower progression to AIDS. **Analysis of Options:** * **Option A (Correct):** Without a functional CCR5 co-receptor, the virus cannot fuse with the host cell membrane, preventing infection. * **Option B:** A mutation (specifically Δ32) leads to resistance, not susceptibility, because the virus loses its binding site. * **Option C:** Resistance to ART is usually due to mutations in the viral genome (e.g., Pol gene mutations affecting Reverse Transcriptase or Protease), not host receptor mutations. * **Option D:** Virulence is a viral property; host receptor mutations affect the host's "permissiveness" to infection rather than the inherent pathogenicity of the virus. **High-Yield Clinical Pearls for NEET-PG:** * **CXCR4:** This is the co-receptor for **T-tropic** strains, which usually appear later in the course of the disease (associated with rapid CD4 decline). * **Maraviroc:** A drug that acts as a **CCR5 antagonist**, mimicking the effect of the mutation to prevent viral entry. * **Berlin Patient:** The first person cured of HIV received a bone marrow transplant from a donor homozygous for the CCR5-Δ32 mutation. * **GP120:** The viral envelope protein that initially binds to CD4 and then undergoes a conformational change to bind to CCR5/CXCR4.

Question 866: Which statement is true about the relative concentrations of immunoglobulins in serum?

A. IgE has the minimum concentration. (Correct Answer)
B. IgG has the minimum concentration.
C. IgA has the minimum concentration.
D. IgM has the minimum concentration.

Explanation: In human serum, the concentration of immunoglobulins follows a specific hierarchy based on their physiological roles and half-lives. The correct order from highest to lowest concentration is **IgG > IgA > IgM > IgD > IgE**. ### Why the Correct Answer is Right **IgE** is the least abundant immunoglobulin in the serum of healthy individuals, with a concentration of approximately **0.00005 mg/mL** (or <0.001% of total serum Ig). Its low concentration is due to its short half-life (approx. 2 days) and the fact that most IgE is sequestered on the surface of mast cells and basophils via high-affinity FcεRI receptors, rather than circulating freely. ### Why the Other Options are Wrong * **IgG (Option B):** This is the **most abundant** immunoglobulin (75–80% of total serum Ig), providing long-term immunity and the only class that crosses the placenta. * **IgA (Option C):** This is the **second most abundant** serum immunoglobulin (10–15%). It is the primary antibody found in secretions (colostrum, saliva, tears). * **IgM (Option D):** This is the **third most abundant** (5–10%). It is a pentamer and the first antibody produced during a primary immune response. ### NEET-PG High-Yield Pearls * **Mnemonic for Concentration:** **GAMDE** (IgG > IgA > IgM > IgD > IgE). * **IgG:** Longest half-life (23 days); responsible for secondary immune response. * **IgM:** Highest molecular weight (Millionaire antibody); best for complement fixation. * **IgA:** Most produced antibody *per day* in the body (due to mucosal surface area), but serum levels are second to IgG. * **IgE:** Levels significantly increase in **Type I Hypersensitivity** (allergies) and **helminthic (parasitic) infections**.

Question 867: Passive cutaneous anaphylaxis is detected by which of the following?

A. Heterocytotropic antibody (Correct Answer)
B. Wheal and flare reaction
C. Atopy
D. Cutaneous anaphylaxis

Explanation: **Explanation:** **Passive Cutaneous Anaphylaxis (PCA)** is an in vivo method used to detect and measure antibodies (primarily IgE) responsible for Type I hypersensitivity. **Why Option A is correct:** The test involves injecting serum containing antibodies from one species (e.g., human) into the skin of an animal of a different species (e.g., guinea pig). These antibodies are called **Heterocytotropic antibodies** because they have an affinity for the mast cells of a different species. After a latent period (allowing the antibodies to fix to mast cells), the specific antigen is injected intravenously along with a dye (Evans blue). If the antibody is present, an antigen-antibody reaction occurs, triggering mast cell degranulation. This increases vascular permeability, causing the dye to leak into the tissues, appearing as a blue spot. **Why other options are incorrect:** * **B. Wheal and flare reaction:** This is the clinical manifestation of an *active* Type I hypersensitivity skin test (like the Prick test) in a sensitized individual, not the mechanism of the passive transfer test. * **C. Atopy:** This refers to a genetic predisposition to develop localized Type I hypersensitivity reactions (like asthma or hay fever) to common environmental allergens. * **D. Cutaneous anaphylaxis:** This is a general term for a localized anaphylactic reaction in the skin; it does not describe the specific laboratory detection method involving heterocytotropic antibodies. **High-Yield Pearls for NEET-PG:** * **Homocytotropic antibodies:** Antibodies (IgE) that bind to mast cells of the *same* species. * **Prausnitz-Küstner (PK) Reaction:** A historical method of passive transfer using homocytotropic antibodies (human to human). It is no longer used due to the risk of transmitting infections like Hepatitis and HIV. * **Latent Period:** Essential in PCA to allow the injected antibodies to fix to the Fc receptors on mast cells while the circulating non-specific antibodies are cleared.

Question 868: Which of the immunoglobulins is primarily found in Peyer's patches?

A. IgM
B. IgG
C. IgA (Correct Answer)
D. IgD

Explanation: **Explanation:** The correct answer is **IgA**. **Underlying Concept:** Peyer’s patches are organized lymphoid tissues located in the lamina propria of the small intestine, forming a critical part of the **Mucosa-Associated Lymphoid Tissue (MALT)**. Their primary function is to monitor intestinal bacteria and prevent the growth of pathogenic microorganisms. **IgA** (specifically secretory IgA) is the predominant antibody class produced at mucosal surfaces. Within Peyer’s patches, B-cells undergo class-switching to become IgA-producing plasma cells, which then secrete dimeric IgA to neutralize pathogens before they can penetrate the intestinal epithelium. **Analysis of Incorrect Options:** * **IgM:** While IgM is the first antibody produced in a primary immune response and can be secreted across mucosa, it is not the primary resident of Peyer’s patches. * **IgG:** This is the most abundant immunoglobulin in the **serum** and provides systemic immunity. It reaches mucosal surfaces primarily via passive diffusion rather than local production in MALT. * **IgD:** This is primarily found on the surface of B-lymphocytes as an antigen receptor; it has no significant role in mucosal defense. **Clinical Pearls for NEET-PG:** * **Secretory Component:** IgA acquires a "secretory component" (derived from the poly-Ig receptor) which protects it from digestion by intestinal enzymes. * **Selective IgA Deficiency:** The most common primary immunodeficiency; patients often present with recurrent sinopulmonary and GI infections (e.g., *Giardia lamblia*). * **M-Cells:** Specialized cells in the epithelium overlying Peyer’s patches that transport antigens from the gut lumen to the underlying lymphoid tissue.

Question 869: Amniocentesis conducted during genetic counseling of a pregnant woman reveals a fetal adenosine deaminase deficiency. This autosomal recessive immunodeficiency is usually associated with which of the following?

A. Humoral Immunity - Normal; Cellular Immunity - Normal
B. Humoral Immunity - Normal; Cellular Immunity - Deficient
C. Humoral Immunity - Deficient; Cellular Immunity - Normal
D. Humoral Immunity - Deficient; Cellular Immunity - Deficient (Correct Answer)

Explanation: ### Explanation **Adenosine Deaminase (ADA) deficiency** is the second most common cause of **Severe Combined Immunodeficiency (SCID)**, accounting for approximately 15% of cases. It is inherited as an autosomal recessive trait. #### Why Option D is Correct: The enzyme adenosine deaminase is essential for the purine salvage pathway. Its deficiency leads to the accumulation of toxic metabolites, specifically **deoxyadenosine** and **dATP**, within lymphocytes. These metabolites are lymphotoxic; they inhibit DNA synthesis and induce apoptosis. Because this metabolic defect affects the common lymphoid progenitor cell line, it results in the failure of both **T-cell and B-cell maturation**. Consequently, patients exhibit a profound lack of both **Cellular Immunity** (T-cells) and **Humoral Immunity** (B-cells/Antibodies). #### Why Other Options are Incorrect: * **Option A:** This describes an immunocompetent state. ADA deficiency is a primary immunodeficiency. * **Option B:** This pattern (Deficient Cellular, Normal Humoral) is characteristic of **DiGeorge Syndrome** (thymic hypoplasia), where T-cells are low but B-cells are initially preserved. * **Option C:** This pattern (Deficient Humoral, Normal Cellular) is characteristic of **X-linked Agammaglobulinemia (Bruton’s)**, where B-cell maturation is blocked but T-cell function remains intact. #### NEET-PG High-Yield Pearls: * **SCID Presentation:** Recurrent "failure to thrive," chronic diarrhea, and severe opportunistic infections (e.g., *Pneumocystis jirovecii*, *Candida*) in early infancy. * **Imaging:** Characteristically shows an **absent thymic shadow** on chest X-ray. * **Historical Significance:** ADA deficiency was the first disease treated with **Gene Therapy**. * **Treatment:** Hematopoietic stem cell transplant (HSCT) is the treatment of choice; Enzyme Replacement Therapy (PEG-ADA) is a temporizing measure.

Question 870: Which marker is lineage-specific for B cells?

A. CD 19 (Correct Answer)
B. CD 20
C. CD 21
D. CD 22

Explanation: **Explanation:** The correct answer is **CD 19**. **Why CD 19 is the correct answer:** CD 19 is considered the most reliable **lineage-specific marker** for B cells because it is expressed from the earliest stages of B-cell commitment (pro-B cell) through all stages of maturation, until it is finally downregulated during terminal differentiation into plasma cells. Because it appears before other markers and is present on almost all B-lineage cells, it is the gold standard for identifying B cells in flow cytometry. **Analysis of Incorrect Options:** * **CD 20:** While highly specific to B cells, it is not expressed on the earliest pro-B cells. It is primarily found on mature B cells and is lost during the transition to plasma cells. (Clinical Note: It is the target for **Rituximab**). * **CD 21:** Also known as Complement Receptor 2 (CR2), it is the receptor for the **Epstein-Barr Virus (EBV)**. It is expressed only on mature B cells and follicular dendritic cells, making it less "lineage-encompassing" than CD 19. * **CD 22:** This is a regulatory molecule appearing later in B-cell maturation (mature B cells) and is not present on the earliest precursors. **High-Yield NEET-PG Pearls:** * **Pan B-cell markers:** CD 19, CD 20, and CD 22. * **Plasma Cell Markers:** CD 138 (Syndecan-1) and CD 38. Note that plasma cells typically **lose** CD 19 and CD 20. * **T-cell Lineage Marker:** CD 3 is the definitive lineage-specific marker for T cells. * **NK Cell Markers:** CD 16 and CD 56. * **Hairy Cell Leukemia:** Characterized by CD 11c, CD 25, and CD 103.

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