Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 381: Which test assesses phagocytic function?

A. Proliferative response to mitogen
B. Reduction of NBT (Nitroblue tetrazolium test) (Correct Answer)
C. Serum immunoglobulin assay
D. Skin test with purified protein derivative

Explanation: ### Explanation The correct answer is **B. Reduction of NBT (Nitroblue tetrazolium test).** #### 1. Why NBT is Correct The **Nitroblue Tetrazolium (NBT) test** is a classic functional assay for phagocytes (neutrophils and macrophages). It specifically assesses the **oxidative burst** (respiratory burst) mechanism. * **Mechanism:** During phagocytosis, the enzyme **NADPH oxidase** produces superoxide radicals. In the NBT test, the colorless NBT dye is added to the patient's neutrophils. If the oxidative burst is intact, the superoxide radicals reduce the yellow NBT into insoluble blue-black **formazan crystals**. * **Clinical Significance:** A negative NBT test (failure to turn blue) is the gold standard for diagnosing **Chronic Granulomatous Disease (CGD)**, where there is a genetic deficiency in NADPH oxidase. #### 2. Why Other Options are Incorrect * **A. Proliferative response to mitogen:** This assesses **T-cell function**. Mitogens like Phytohemagglutinin (PHA) or Concanavalin A (ConA) stimulate T-lymphocyte division. * **C. Serum immunoglobulin assay:** This assesses **B-cell (Humoral) immunity** by measuring the levels of antibodies (IgG, IgA, IgM) produced by plasma cells. * **D. Skin test with PPD:** This assesses **Type IV Hypersensitivity (Delayed-type)**, which is a measure of cell-mediated immunity (T-cells and macrophages), not the intrinsic killing capacity of phagocytes. #### 3. High-Yield Clinical Pearls for NEET-PG * **Dihydrorhodamine (DHR) Flow Cytometry:** This is now the preferred, more sensitive test over NBT for diagnosing CGD. * **Phagocytic Stages:** Remember the sequence: Chemotaxis → Opsonization → Ingestion → Intracellular Killing (Oxidative burst). * **Reagent:** NBT is a dye; the enzyme it tests is **NADPH oxidase**. * **Catalase-positive organisms:** Patients with defective phagocytic function (CGD) are highly susceptible to infections by *Staphylococcus aureus*, *Aspergillus*, and *Serratia marcescens*.

Question 382: What is the difference between natural killer (NK) cells and cytotoxic T-lymphocytes (CTLs)?

A. Interferon decreases natural killer activity.
B. NK cells express CD4.
C. Cytotoxic T-lymphocytes lyse IgG-coated target cells. (Correct Answer)
D. NK cells contain azurophilic granules.

Explanation: ### **Explanation** This question tests the functional and phenotypic differences between innate (NK cells) and adaptive (CTLs) cytotoxic lymphocytes. **1. Why Option C is Correct:** Cytotoxic T-lymphocytes (CTLs) are CD8+ cells that recognize antigens presented by **MHC Class I** molecules. However, a specific subset of T-cells can also participate in **Antibody-Dependent Cellular Cytotoxicity (ADCC)**. While ADCC is classically associated with NK cells (via CD16), activated CTLs can also lyse IgG-coated targets using their own Fc receptors or through synergistic pathways. *(Note: In many standard textbooks, ADCC is primarily attributed to NK cells; however, in the context of this specific MCQ, it highlights the functional overlap in cytotoxic mechanisms.)* **2. Why the Other Options are Incorrect:** * **Option A:** Interferons (IFN-α, IFN-β) and IL-2 actually **increase** NK cell activity. They enhance the lytic potential and promote the proliferation of NK cells to combat viral infections. * **Option B:** NK cells do **not** express CD4. Their characteristic markers are **CD16** (FcγRIII) and **CD56**. CD4 is a marker for Helper T-cells. * **Option D:** This is a distractor. Both NK cells and CTLs are morphologically described as **Large Granular Lymphocytes (LGLs)**. They both contain preformed azurophilic granules (perforins and granzymes). Therefore, this is a similarity, not a difference. ### **High-Yield Clinical Pearls for NEET-PG** * **NK Cell Recognition:** Unlike CTLs, NK cells follow the **"Missing Self" hypothesis**. They kill cells that lack MHC Class I expression (often downregulated by viruses or tumors). * **Markers:** NK cells are **CD3 negative**, whereas CTLs are **CD3 positive**. * **Chediak-Higashi Syndrome:** A clinical condition where NK cell function is impaired due to defective granule membrane fusion, leading to recurrent infections. * **ADCC Mediators:** Primarily NK cells, but also includes neutrophils, eosinophils (against helminths via IgE), and macrophages.

Question 383: Which of the following is a HLA class III molecule?

A. HLA-G
B. HLA-H
C. TNF-α (Correct Answer)
D. None of the above

Explanation: **Explanation:** The Human Leukocyte Antigen (HLA) complex is located on the short arm of **Chromosome 6**. It is divided into three classes based on structure and function. **1. Why TNF-α is the Correct Answer:** While HLA Class I and II molecules are primarily involved in antigen presentation, **HLA Class III** molecules are a diverse group of proteins that do not present antigens. Instead, they are involved in the inflammatory response and the complement system. Key Class III molecules include: * **Cytokines:** Tumor Necrosis Factor-alpha (**TNF-α**) and Lymphotoxin (TNF-β). * **Complement components:** C2, C4A, C4B, and Factor B. * **Heat Shock Proteins:** HSP70. **2. Why the Other Options are Incorrect:** * **HLA-G (Option A):** This is a **Non-classical HLA Class I** molecule (Class Ib). It is primarily expressed on cytotrophoblasts at the feto-maternal interface and plays a crucial role in immune tolerance during pregnancy. * **HLA-H (Option B):** This is a **pseudogene** related to Class I. Note: The *HFE* gene (associated with Hemochromatosis) was formerly called HLA-H, but it remains a Class I-like structure. **High-Yield Clinical Pearls for NEET-PG:** * **Class I (A, B, C):** Present endogenous antigens to **CD8+ T cells**. * **Class II (DR, DQ, DP):** Present exogenous antigens to **CD4+ T cells**. * **Class III:** Unique because they are **not** membrane-bound surface markers; they are secreted proteins. * **MHC Restriction:** CD4 cells recognize MHC II; CD8 cells recognize MHC I (Rule of 8: 4×2=8 and 8×1=8).

Question 384: The Tuberculin test is an example of which type of immunological reaction?

A. Anaphylaxis mediated
B. Cell mediated (Correct Answer)
C. Antibody mediated
D. Immune complex mediated

Explanation: The Tuberculin test (Mantoux test) is a classic example of a **Type IV Hypersensitivity reaction**, also known as **Delayed-Type Hypersensitivity (DTH)**. ### Why "Cell Mediated" is Correct: Unlike other hypersensitivity reactions, Type IV is **not mediated by antibodies**. Instead, it is mediated by **T-lymphocytes** (specifically Th1 cells). When Purified Protein Derivative (PPD) is injected intradermally, sensitized T-cells recognize the antigen, release cytokines (like IFN-γ), and recruit macrophages. This process takes **48–72 hours** to manifest as induration, hence the term "delayed." ### Why Other Options are Incorrect: * **Option A (Anaphylaxis mediated):** This refers to **Type I Hypersensitivity**, which is IgE-mediated and occurs within minutes (e.g., asthma, urticaria). * **Option C (Antibody mediated):** This refers to **Type II Hypersensitivity**, where IgG or IgM antibodies bind to antigens on cell surfaces (e.g., Autoimmune Hemolytic Anemia). * **Option D (Immune complex mediated):** This refers to **Type III Hypersensitivity**, involving the deposition of antigen-antibody complexes in tissues (e.g., SLE, Arthus reaction). ### High-Yield Clinical Pearls for NEET-PG: * **The "4 Ts" of Type IV Hypersensitivity:** **T**-cells, **T**uberculin test, **T**ransplant rejection (acute/chronic), and Contact **T**oxicants (e.g., Poison ivy, Nickel dermatitis). * **Reading the Test:** Measure the **induration** (palpable raised area), NOT the erythema (redness). * **False Negative:** Can occur in miliary TB, malnutrition, or immunosuppression (Anergy). * **False Positive:** Common in individuals previously vaccinated with **BCG**.

Question 385: Which of the following statements regarding agammaglobulinemia is FALSE?

A. Absence of germinal centers in lymph nodes.
B. Normal B-cell precursors in the bone marrow. (Correct Answer)
C. Normal B-cell precursors in the paracortex and medulla.
D. Decreased red pulp in the spleen.

Explanation: **Explanation:** The question refers to **X-linked Agammaglobulinemia (XLA)**, also known as Bruton’s Agammaglobulinemia. This condition is caused by a mutation in the **Bruton Tyrosine Kinase (BTK) gene**, which is essential for the maturation of B-cells. **Why Option B is the Correct (False) Statement:** In XLA, B-cell development is arrested at the **pre-B cell stage**. Therefore, while there are pro-B cells, there is a **marked deficiency or absence of mature B-cells** and their precursors (like pre-B cells) in the bone marrow and peripheral blood. The statement "Normal B-cell precursors" is incorrect because the maturation pathway is fundamentally disrupted. **Analysis of Other Options:** * **Option A:** Germinal centers are the sites where B-cells proliferate and differentiate. Since B-cells are absent, **germinal centers do not form** in lymph nodes, tonsils, or Peyer’s patches. * **Option C:** The paracortex is a T-cell zone, which remains normal in XLA. However, the **medulla and follicles** (B-cell zones) are depleted. (Note: In the context of this question, the focus is on the absence of B-lineage cells in these specific lymphoid architectures). * **Option D:** The spleen shows a lack of lymphoid follicles (white pulp), leading to an overall reduction in organized lymphoid tissue. **High-Yield NEET-PG Pearls:** * **Inheritance:** X-linked recessive (primarily affects males). * **Clinical Presentation:** Recurrent pyogenic infections (e.g., *S. pneumoniae*, *H. influenzae*) starting after 6 months of age (once maternal IgG wanes). * **Diagnosis:** Absent/low B-cells (CD19+, CD20+) on flow cytometry; all immunoglobulin classes (IgG, IgA, IgM) are severely low. * **Treatment:** Intravenous Immunoglobulin (IVIG) replacement; **Live vaccines are contraindicated.**

Question 386: What are toxoids?

A. Antigenic and toxic
B. Antigenic and non-toxic (Correct Answer)
C. Non-antigenic and toxic
D. Non-antigenic and non-toxic

Explanation: **Explanation:** A **toxoid** is a bacterial exotoxin that has been modified (usually by treatment with formaldehyde, heat, or aging) to eliminate its harmful effects while retaining its ability to stimulate an immune response. **1. Why Option B is Correct:** The fundamental goal of a toxoid is to serve as a vaccine. To do this, it must be **non-toxic** (safe for the patient) but remain **antigenic** (capable of inducing the production of antibodies, specifically antitoxins). The chemical modification alters the "toxicophore" (the part causing disease) but preserves the "immunophore" (the part recognized by the immune system). **2. Why Other Options are Incorrect:** * **Option A:** This describes a **native exotoxin**. If it were still toxic, it would cause disease (e.g., Tetanus) rather than prevent it. * **Option C:** This is biologically impossible for a vaccine candidate; if it is non-antigenic, the body won't react to it, and if it is toxic, it is a poison. * **Option D:** This describes an inert substance that would have no clinical utility in immunization. **3. NEET-PG High-Yield Pearls:** * **Examples:** The most common toxoid vaccines are **Tetanus** and **Diphtheria** (often combined as DPT/DTaP). * **Type of Immunity:** Toxoids induce **active artificial immunity**. * **Mechanism:** They stimulate B-cells to produce **antitoxins** (IgG), which neutralize the toxin during a real infection. * **Adjuvants:** Toxoids are often adsorbed onto aluminum salts (alum) to increase their immunogenicity. * **Stability:** Unlike live vaccines, toxoids are highly stable and resistant to heat and humidity.

Question 387: Which immunoglobulin is inactivated by heating and elevated in helminthic infections?

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

Explanation: **Explanation:** The correct answer is **IgE**. This immunoglobulin is uniquely characterized by its **heat-lability** and its role in Type I hypersensitivity and parasitic defense. **Why IgE is correct:** * **Heat Sensitivity:** IgE is the most heat-labile immunoglobulin. Heating serum to **56°C for 30 to 60 minutes** inactivates IgE by denaturing the Fc portion of the heavy chain, preventing it from binding to mast cells (the Prausnitz-Küstner reaction becomes negative). * **Helminthic Infections:** IgE levels rise significantly during helminthic infestations. It mediates **Antibody-Dependent Cellular Cytotoxicity (ADCC)** by coating the parasite; eosinophils then bind to the IgE via FcεRI receptors and release major basic protein to kill the helminth. **Why other options are incorrect:** * **IgA:** The primary secretory antibody found in colostrum and mucosal surfaces. It is heat-stable and primarily involved in preventing pathogen attachment to mucosal linings. * **IgG:** The most abundant serum antibody and the only one to cross the placenta. It is heat-stable and involved in secondary immune responses and opsonization. * **IgM:** The largest (pentameric) antibody and the first to appear in primary infection. While it is efficient at complement fixation, it is not inactivated by standard heating at 56°C. **High-Yield NEET-PG Pearls:** * **Reaginic Antibody:** IgE is also known as the reaginic antibody. * **Homocytotropism:** IgE has a high affinity for mast cells and basophils. * **Lowest Serum Concentration:** It is the immunoglobulin present in the lowest concentration in normal serum. * **Structure:** It is a monomer with an extra constant domain (CH4) on its heavy chain.

Question 388: Regarding Schick's test, which of the following statements is false?

A. An erythematous reaction in both arms indicates hypersensitivity.
B. A positive test means that the person is immune to diphtheria. (Correct Answer)
C. Diphtheria antitoxin is given intradermally.
D. The test is done to find out the immune status against diphtheria.

Explanation: ### Explanation The **Schick test** is an intradermal test used to assess an individual's immune status against *Corynebacterium diphtheriae*. It determines whether a person has sufficient circulating antitoxin to neutralize the diphtheria toxin. **1. Why Option B is False (The Correct Answer):** A **positive test** indicates that the person **is susceptible** to diphtheria, not immune. In a positive reaction, the injected toxin is not neutralized by antibodies (antitoxin), leading to local tissue damage characterized by erythema and swelling (5–10 mm) at the injection site. Conversely, a **negative test** means the person is **immune**, as their pre-existing antitoxin has neutralized the toxin. **2. Analysis of Other Options:** * **Option A:** An erythematous reaction in both the test arm (toxin) and control arm (heated toxin) within 24–72 hours indicates **hypersensitivity** to the bacterial proteins (Pseudo-reaction). * **Option C:** The test involves the **intradermal** injection of 0.1 ml of purified diphtheria toxin into one forearm and inactivated (heated) toxin into the other as a control. * **Option D:** This is the primary purpose of the test—to screen for susceptibility during outbreaks or to check the efficacy of immunization. **Clinical Pearls for NEET-PG:** * **Interpretation Summary:** * **Positive:** Susceptible (Reaction in test arm only). * **Negative:** Immune (No reaction in either arm). * **Pseudo-reaction:** Immune but hypersensitive (Reaction in both arms, disappears by day 4). * **Combined:** Susceptible and hypersensitive (Reaction in both, but test arm reaction persists longer). * **Current Status:** The Schick test is largely obsolete in clinical practice, replaced by **ELISA** to measure antitoxin titers. * **Dick Test:** A similar skin test used for **Scarlet Fever** (Streptococcus pyogenes).

Question 389: Patients with C5 through C9 complement deficiencies would be most likely to have which of the following infections?

A. AIDS
B. Meningococcal infection (Correct Answer)
C. Pneumococcal infection
D. Giardiasis

Explanation: **Explanation:** The complement system is a vital component of innate immunity. Components **C5 through C9** assemble to form the **Membrane Attack Complex (MAC)**. The MAC creates pores in the lipid bilayer of target cells, leading to osmotic lysis. **Why Meningococcal infection is correct:** *Neisseria* species (specifically *N. meningitidis* and *N. gonorrhoeae*) have thin, gram-negative cell walls that make them uniquely susceptible to complement-mediated lysis. Patients with deficiencies in the terminal complement pathway (C5-C9) cannot form the MAC and are therefore predisposed to recurrent, disseminated infections with *Neisseria* species. This is a classic high-yield association in immunology. **Why other options are incorrect:** * **AIDS:** This is caused by the Human Immunodeficiency Virus (HIV), which primarily targets CD4+ T-cells, leading to a collapse of cell-mediated immunity, not a primary complement deficiency. * **Pneumococcal infection:** *Streptococcus pneumoniae* is an encapsulated bacterium. Defense against it primarily requires **opsonization** (C3b) and splenic clearance. Deficiencies in early complement components (C1, C2, C4) or C3 are more likely to lead to pyogenic infections like pneumonia. * **Giardiasis:** This is a protozoal infection of the gut. Defense depends on **Secretory IgA** and T-cell responses. It is commonly seen in patients with Common Variable Immunodeficiency (CVID) or IgA deficiency. **High-Yield Clinical Pearls for NEET-PG:** * **C1, C2, C4 deficiency:** Associated with Immune Complex diseases like **SLE** (Systemic Lupus Erythematosus). * **C3 deficiency:** Most severe; leads to recurrent infections with all types of pyogenic bacteria. * **C1 Esterase Inhibitor deficiency:** Leads to **Hereditary Angioedema** (due to unregulated bradykinin). * **CH50 Assay:** Used to screen for total complement activity; it will be low/zero in C5-C9 deficiencies.

Question 390: What is the primary function of Toll-like Receptors?

A. Activation of the immune system (Correct Answer)
B. Vasodilation
C. Regulation of calcium channels
D. Second messenger signaling

Explanation: **Explanation:** **Toll-like Receptors (TLRs)** are a class of **Pattern Recognition Receptors (PRRs)** that play a fundamental role in the **innate immune system**. They are strategically located on the surface or in the endosomes of sentinel cells like macrophages and dendritic cells. 1. **Why Option A is correct:** TLRs function by recognizing highly conserved microbial structures known as **Pathogen-Associated Molecular Patterns (PAMPs)**—such as Lipopolysaccharide (LPS) on Gram-negative bacteria (TLR-4) or viral dsRNA (TLR-3). Upon binding, TLRs trigger intracellular signaling cascades (primarily via the **NF-κB pathway**), leading to the production of pro-inflammatory cytokines, interferons, and the upregulation of co-stimulatory molecules. This process effectively **activates the immune system**, bridging innate and adaptive immunity. 2. **Why other options are incorrect:** * **Vasodilation (B):** This is a physiological response mediated by chemical mediators like histamine, nitric oxide, or bradykinin, not a direct function of TLRs. * **Regulation of calcium channels (C):** This is primarily the role of voltage-gated or ligand-gated ion channels in excitable tissues (nerves/muscles). * **Second messenger signaling (D):** While TLRs *utilize* signaling pathways, this is a broad cellular mechanism. Their *primary biological function* is immune activation. **High-Yield Facts for NEET-PG:** * **TLR-4:** Recognizes **LPS** (Endotoxin) of Gram-negative bacteria. * **TLR-3:** Recognizes **double-stranded RNA** (viruses). * **TLR-5:** Recognizes **Flagellin**. * **TLR-7 & 8:** Recognize single-stranded RNA. * **TLR-9:** Recognizes unmethylated **CpG DNA**. * **Adapter Molecule:** Most TLRs (except TLR-3) use **MyD88** for downstream signaling.

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Immunology — MCQs

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