Immunology — MCQs

A young girl has had repeated infections with Candida albicans and respiratory viruses since 3 months of age. As part of the clinical evaluation of her immune status, her responses to routine immunization procedures should be tested. In this evaluation, the use of which of the following vaccines is contraindicated?

Q897Medium

An 11-year-old boy presents with multiple abscesses on his face, chest, and back, along with a history of recurrent respiratory infections. Physical examination reveals atopic excoriating skin and multiple cold abscesses on his back. What is the most probable diagnosis?

Q898Easy

Which of the following complement components attaches to the crystallizable fragment of immunoglobulin M?

Q899Easy

The Oakley-Fulthorpe procedure involves which of the following?

Q900Easy

Which of the following statements accurately describes Natural Killer (NK) cells?

Immunology Indian Medical PG Practice Questions and MCQs

Question 891: Which of the following is an example of a precipitation reaction?

A. Widal Test
B. Coomb's Test
C. Counter Current Immunoelectrophoresis (Correct Answer)
D. Weil-Felix Test

Explanation: **Explanation:** The fundamental principle of a **precipitation reaction** is the interaction between a **soluble antigen** and a **soluble antibody** to form an insoluble visible complex (lattice) in the presence of electrolytes at an optimal temperature and pH. **Why Option C is correct:** **Counter Current Immunoelectrophoresis (CIEP)** is a rapid form of precipitation in gel. It utilizes an electric current to drive the antigen and antibody toward each other. The antigen (usually negatively charged) moves toward the anode, while the antibody moves toward the cathode due to electroendosmosis. When they meet in optimal proportions, a visible **precipitation line** forms. It is significantly faster and more sensitive than standard radial immunodiffusion. **Why other options are incorrect:** * **Widal Test (A) and Weil-Felix Test (D):** These are examples of **Direct Agglutination** reactions. In agglutination, the antigen is **particulate/insoluble** (e.g., whole bacterial cells like *Salmonella* or *Proteus*). When they react with antibodies, they form visible clumps rather than precipitates. * **Coombs’ Test (B):** This is an **Antiglobulin Test** (Indirect Agglutination). It uses antihuman globulin to detect "incomplete" antibodies that are already coated on the surface of Red Blood Cells but are unable to cause visible agglutination on their own. **NEET-PG High-Yield Pearls:** * **Precipitation** = Soluble Ag + Soluble Ab. * **Agglutination** = Particulate Ag + Soluble Ab. * **VDRL & Kahn Test:** Classic examples of **Flocculation** (a subtype of precipitation where the precipitate remains suspended as flakes). * **Elek’s Test:** A specialized precipitation test (toxigenicity test) used for *Corynebacterium diphtheriae*. * **Zone Phenomenon:** Precipitation is most visible in the **Zone of Equivalence**. Excess of either antibody (Prozone) or antigen (Postzone) can lead to false-negative results.

Question 892: Which of the following immunoglobulins acts as a receptor for antigens?

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

Explanation: ### Explanation **Correct Option: C (IgD)** The primary function of **IgD** is to act as an **antigen receptor** on the surface of mature, naive B-lymphocytes. Along with monomeric IgM, IgD is co-expressed on the B-cell membrane before the cell has encountered its specific antigen. When an antigen binds to these surface receptors, it triggers B-cell activation, leading to clonal expansion and differentiation into plasma cells. Unlike other immunoglobulins, IgD is secreted in very trace amounts in the serum and has no well-defined effector function (like opsonization or complement activation) once secreted. **Incorrect Options:** * **IgG:** This is the most abundant serum immunoglobulin. Its primary roles are opsonization, complement activation, and providing passive immunity to the fetus (crosses the placenta). It does not serve as a primary B-cell receptor. * **IgM:** While the **monomeric** form of IgM acts as a B-cell receptor alongside IgD, the **pentameric** form is the first antibody produced in a primary immune response and is highly effective at complement fixation. * **IgE:** This immunoglobulin is primarily involved in Type I hypersensitivity reactions (allergy) and provides immunity against helminthic parasites by binding to Fc receptors on mast cells and basophils. **High-Yield Clinical Pearls for NEET-PG:** * **B-cell Markers:** Mature naive B-cells are characterized by the presence of both **surface IgM and IgD**. * **Heat Lability:** IgD and IgE are the most heat-labile immunoglobulins. * **Hinge Region:** IgD has the longest hinge region, making it highly susceptible to proteolytic degradation. * **Memory B-cells:** Once a B-cell undergoes class switching (e.g., to IgG), it loses the expression of IgD.

Question 893: Delayed tuberculin test response is due to:

A. B lymphocytes
B. T lymphocytes (Correct Answer)
C. Monocytes
D. Histiocytes

Explanation: **Explanation:** The tuberculin test (Mantoux test) is the classic clinical example of a **Type IV Hypersensitivity reaction**, also known as **Delayed-Type Hypersensitivity (DTH)**. **Why T lymphocytes are correct:** The reaction is mediated by **T lymphocytes**, specifically CD4+ Th1 cells. When tuberculin antigen (PPD) is injected intradermally in a previously sensitized individual, memory T cells recognize the antigen. These cells then release cytokines (such as IFN-γ and IL-2), which recruit and activate macrophages. This process takes time to develop, which is why the induration is read **48 to 72 hours** after the injection—hence the term "delayed." **Why other options are incorrect:** * **B lymphocytes:** These are responsible for Type I, II, and III hypersensitivity reactions via the production of antibodies. Type IV reactions are strictly cell-mediated and do not involve antibodies. * **Monocytes/Histiocytes:** While monocytes (which differentiate into macrophages/histiocytes) are the primary effector cells that cause the actual tissue swelling and induration, they are **recruited and directed** by T lymphocytes. The "response" or the immunological memory that triggers the test is fundamentally a T-cell function. **NEET-PG High-Yield Pearls:** * **Key Cytokine:** IFN-γ (Interferon-gamma) is the most critical cytokine in this reaction. * **Histology:** The hallmark of a positive test is the perivascular accumulation of "cuffing" by mononuclear cells (lymphocytes and macrophages). * **False Negatives:** Can occur in patients with miliary TB, sarcoidosis, malnutrition, or immunosuppression (e.g., HIV/AIDS) due to **anergy** (loss of T-cell reactivity). * **Other Type IV Examples:** Contact dermatitis (poison ivy, nickel), Granuloma formation, and Lepromin test.

Question 894: Which of the following is a lineage-specific T cell marker?

A. CD 1
B. CD 19
C. CD 3 (Correct Answer)
D. CD 4

Explanation: **Explanation:** **CD3** is the definitive lineage-specific marker for **T lymphocytes**. It is a multi-protein complex covalently associated with the T-cell receptor (TCR). Its primary function is signal transduction following antigen recognition. CD3 is expressed on all mature T cells (both Helper and Cytotoxic) and is first detected during the early stages of thymocyte development, making it the most reliable marker for identifying cells of T-cell lineage. **Analysis of Incorrect Options:** * **CD1:** This is a family of glycoproteins structurally related to MHC molecules. They are primarily expressed on **Antigen Presenting Cells (APCs)**, such as dendritic cells and Langerhans cells, and are involved in presenting lipid antigens to NKT cells. * **CD19:** This is the classic lineage-specific marker for **B lymphocytes**. It is expressed from the pro-B cell stage until just before terminal differentiation into plasma cells. * **CD4:** While found on T cells, it is **not lineage-specific**. It is a co-receptor specific to the **Helper T cell subset** (MHC II restricted). Furthermore, CD4 is also expressed on the surface of monocytes and macrophages, which are not of the T-cell lineage. **High-Yield Clinical Pearls for NEET-PG:** * **Pan-T cell markers:** CD2, CD3, CD5, and CD7. * **Pan-B cell markers:** CD19, CD20, and CD21. * **NK cell markers:** CD16 (FcγRIII) and CD56. * **Flow Cytometry:** CD3 is used in clinical practice to differentiate T-cell acute lymphoblastic leukemia (T-ALL) from B-cell lineages. * **Abatacept/Muromonab-CD3:** Historically, OKT3 was a therapeutic monoclonal antibody targeting CD3 used to prevent transplant rejection.

Question 895: A patch test is what type of hypersensitivity?

A. Type 4 (Correct Answer)
B. Type 1
C. Type 2
D. Type 3

Explanation: **Explanation:** The correct answer is **Type 4 Hypersensitivity**, also known as **Delayed-Type Hypersensitivity (DTH)**. **Why Type 4 is correct:** A patch test is the gold standard for diagnosing **Allergic Contact Dermatitis** (e.g., sensitivity to nickel, poison ivy, or cosmetics). Unlike other hypersensitivities, Type 4 is **cell-mediated**, involving T-lymphocytes (specifically Th1 cells and CD8+ T-cells) rather than antibodies. When an allergen is applied to the skin via a patch, sensitized T-cells take **48 to 72 hours** to migrate to the site and release cytokines, causing a localized inflammatory response (induration and erythema). This delay in reaction is why it is termed "delayed." **Why other options are incorrect:** * **Type 1 (Immediate):** Mediated by **IgE antibodies** and mast cell degranulation (e.g., Anaphylaxis, Asthma). Reactions occur within minutes. The diagnostic test for this is the **Skin Prick Test**, not the Patch Test. * **Type 2 (Cytotoxic):** Mediated by **IgG or IgM** antibodies directed against antigens on cell surfaces (e.g., Rheumatic fever, Goodpasture syndrome). * **Type 3 (Immune-Complex):** Caused by the deposition of **antigen-antibody complexes** in tissues (e.g., SLE, Serum sickness, Arthus reaction). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Hypersensitivity (Gell & Coombs):** **ACID** (Type 1: **A**llergic/Anaphylactic; Type 2: **C**ytotoxic; Type 3: **I**mmune-complex; Type 4: **D**elayed). * **Other Type 4 examples:** Mantoux (Tuberculin) test, Lepromin test, Graft rejection, and Granuloma formation (Sarcoidosis, TB). * **Key Cells:** Type 4 is the only hypersensitivity that **does not involve antibodies**. It is mediated by T-cells and Macrophages.

Question 896: A young girl has had repeated infections with Candida albicans and respiratory viruses since 3 months of age. As part of the clinical evaluation of her immune status, her responses to routine immunization procedures should be tested. In this evaluation, the use of which of the following vaccines is contraindicated?

A. Diphtheria toxoid
B. Bordetella pertussis vaccine
C. Tetanus toxoid
D. BCG (Correct Answer)

Explanation: **Explanation:** The clinical presentation of repeated infections with *Candida albicans* (fungal) and respiratory viruses starting in early infancy suggests a **T-cell deficiency** or **Severe Combined Immunodeficiency (SCID)**. In patients with compromised cell-mediated immunity (CMI), the administration of **live attenuated vaccines** is strictly contraindicated. **Why BCG is the correct answer:** BCG (Bacillus Calmette-Guérin) is a **live attenuated vaccine** derived from *Mycobacterium bovis*. In a healthy individual, the T-cells and macrophages contain the attenuated bacteria. However, in a child with T-cell deficiency, the body cannot limit the replication of the vaccine strain, leading to "BCG-osis"—a life-threatening, disseminated infection. **Why other options are incorrect:** * **Options A, B, and C (Diphtheria, Pertussis, Tetanus):** These are components of the DPT/DTaP vaccine. Diphtheria and Tetanus are **toxoids** (inactivated toxins), and the Pertussis component is either **killed** (whole-cell) or **acellular** (subunit). Since these vaccines do not contain live replicating organisms, they cannot cause infectious disease in immunocompromised hosts, though the immune response (antibody production) may be suboptimal. **High-Yield Clinical Pearls for NEET-PG:** * **Live Vaccines Contraindicated in Immunodeficiency:** BCG, OPV (Sabin), MMR, Varicella, Rotavirus, and Yellow Fever. * **SCID Presentation:** Usually manifests at 3–6 months of age (as maternal antibodies wane) with failure to thrive, chronic diarrhea, and recurrent opportunistic infections (e.g., *Pneumocystis jirovecii*, *Candida*). * **Safe Alternatives:** Inverted/Killed vaccines (Salk Polio instead of Sabin) and Toxoids are safe as they pose no risk of dissemination.

Question 897: An 11-year-old boy presents with multiple abscesses on his face, chest, and back, along with a history of recurrent respiratory infections. Physical examination reveals atopic excoriating skin and multiple cold abscesses on his back. What is the most probable diagnosis?

A. Hyper IgE syndrome (Correct Answer)
B. Hyper IgM syndrome
C. Carcinoid syndrome
D. Wiskott Aldrich syndrome

Explanation: ### **Explanation** The clinical presentation of recurrent skin and respiratory infections, atopic dermatitis, and the hallmark **"cold abscesses"** (abscesses lacking typical signs of inflammation like warmth or redness) is diagnostic of **Hyper IgE Syndrome (Job Syndrome)**. **1. Why Hyper IgE Syndrome is Correct:** This is a primary immunodeficiency, most commonly caused by a **STAT3 mutation** (Autosomal Dominant). This mutation leads to a failure of Th17 cell differentiation. Since Th17 cells are crucial for recruiting neutrophils to sites of infection, their absence results in a lack of inflammatory response, leading to "cold" staphylococcal abscesses. Laboratory findings typically show **markedly elevated IgE levels** (>2000 IU/mL) and eosinophilia. **2. Why Incorrect Options are Wrong:** * **Hyper IgM Syndrome:** Characterized by a defect in CD40L, leading to an inability to class-switch from IgM. Patients present with recurrent sinopulmonary infections and opportunistic infections (e.g., *Pneumocystis jirovecii*), but not cold abscesses or extreme IgE elevation. * **Carcinoid Syndrome:** A paraneoplastic syndrome (usually from neuroendocrine tumors) presenting with flushing, diarrhea, and wheezing due to serotonin excess. It has no primary immunological basis. * **Wiskott-Aldrich Syndrome:** Defined by the triad of **T**hrombocytopenia (small platelets/bleeding), **E**czema, and **R**ecurrent infections (**mnemonic: WATER**). While it involves eczema, the presence of cold abscesses specifically points toward Hyper IgE. **3. NEET-PG High-Yield Pearls (FATED Mnemonic):** To remember the features of Job Syndrome, use **FATED**: * **F**acies (coarse facial features: prominent forehead, deep-set eyes). * **A**bscesses (Cold Staphylococcal abscesses). * **T**eeth (retention of primary/deciduous teeth). * **E**levated IgE. * **D**ermatological problems (Eczema). * *Bonus:* Fractures from minor trauma are also common.

Question 898: Which of the following complement components attaches to the crystallizable fragment of immunoglobulin M?

A. C5b
B. C5a
C. Clqrs (Correct Answer)
D. C4b2a

Explanation: ### Explanation The correct answer is **C1qrs**. This question tests your understanding of the **Classical Pathway** of the complement system and its initiation. **Why C1qrs is correct:** The classical pathway is triggered by the binding of the **C1 complex** (a macromolecule consisting of C1q, C1r, and C1s) to the **Fc (crystallizable fragment)** portion of an antigen-bound antibody. Specifically, the C1q subunit binds to the CH2 domain of IgG or the **CH3 domain of IgM**. IgM is the most potent activator of the classical pathway because its pentameric structure provides multiple Fc binding sites in close proximity. **Analysis of Incorrect Options:** * **C5b:** This is a fragment generated after C5 cleavage. It serves as the initial component for the assembly of the **Membrane Attack Complex (MAC)** (C5b-C9) and does not bind to antibodies. * **C5a:** This is a small peptide fragment (anaphylatoxin) released into the fluid phase. It is a potent chemoattractant for neutrophils and does not have binding affinity for the Fc region. * **C4b2a:** This is known as the **C3 convertase** of the classical pathway. It is an enzyme complex formed on the surface of the pathogen to cleave C3 into C3a and C3b; it does not bind directly to the antibody. **High-Yield Clinical Pearls for NEET-PG:** * **Potency:** One molecule of **IgM** can activate the classical pathway, whereas at least two molecules of **IgG** (specifically IgG1, IgG2, or IgG3) are required. * **Mnemonic for C1qrs:** **Q** binds the antibody, **R** activates **S** (**Q** → **R** → **S**). * **Calcium Dependency:** The integrity of the C1qrs complex is dependent on **Calcium (Ca²⁺)** ions. * **Inhibitor:** C1-esterase inhibitor (C1-INH) regulates this step; its deficiency leads to **Hereditary Angioedema**.

Question 899: The Oakley-Fulthorpe procedure involves which of the following?

A. Single diffusion in one dimension
B. Double diffusion in one dimension (Correct Answer)
C. Single diffusion in two dimensions
D. Double diffusion in two dimensions

Explanation: The **Oakley-Fulthorpe procedure** is a classic immunodiffusion technique used to detect antigen-antibody reactions. ### **Explanation of the Correct Answer** The Oakley-Fulthorpe procedure is a **Double Diffusion in One Dimension** technique. * **Double Diffusion:** Both the antigen and the antibody move (diffuse) toward each other through a medium. * **One Dimension:** The diffusion occurs vertically in a narrow tube. In this method, the antibody is incorporated into agar at the bottom of a tube, followed by a layer of plain agar (the "spacer"), and the antigen is layered on top. Both reactants diffuse into the central plain agar column. Where they meet in optimal proportions (zone of equivalence), a band of precipitation forms. ### **Why Other Options are Incorrect** * **A. Single diffusion in one dimension:** Known as **Oudin diffusion**. Here, only the antigen moves into a column of agar containing the antibody. * **C. Single diffusion in two dimensions:** Known as **Radial Immunodiffusion (Mancini technique)**. The antibody is incorporated into an agar plate, and the antigen diffuses outward from a central well, forming a ring. * **D. Double diffusion in two dimensions:** Known as **Elek’s test** or **Ouchterlony technique**. Both antigen and antibody diffuse toward each other horizontally on a flat agar surface. ### **High-Yield Clinical Pearls for NEET-PG** * **Elek’s Gel Precipitation Test:** A high-yield application of double diffusion in two dimensions used for detecting the toxigenicity of *Corynebacterium diphtheriae*. * **Mancini Technique:** Used clinically to quantify levels of immunoglobulins (IgG, IgM, IgA) or complement components in serum. * **Precipitation vs. Agglutination:** Remember that precipitation involves **soluble** antigens, whereas agglutination involves **particulate/insoluble** antigens.

Question 900: Which of the following statements accurately describes Natural Killer (NK) cells?

A. NK cells belong to the B-cell lineage.
B. NK cells belong to the T-cell lineage.
C. NK cells display a cytotoxic effect on tumor cells. (Correct Answer)
D. NK cells require previous antigen exposure for activation.

Explanation: **Explanation:** **Natural Killer (NK) cells** are a distinct lineage of large granular lymphocytes that play a critical role in the innate immune system. Unlike T or B cells, they do not possess antigen-specific receptors (TCR or BCR). **Why Option C is correct:** NK cells are specialized to identify and destroy "stressed" cells, such as **tumor cells** and **virus-infected cells**, without prior sensitization. They function via the "Missing Self" hypothesis: they express **Inhibitory Receptors** (e.g., KIR) that recognize MHC Class I molecules on healthy cells. Since many tumor cells downregulate MHC Class I to evade T-cells, NK cells lose this inhibitory signal, trigger their **Activating Receptors**, and release perforins and granzymes to induce apoptosis. **Why other options are incorrect:** * **Options A & B:** NK cells belong to the **Lymphoid lineage** (derived from the Common Lymphoid Progenitor), but they are distinct from B-cells and T-cells. They are often referred to as "Null cells" because they lack traditional B-cell (CD19/20) or T-cell (CD3) surface markers. * **Option D:** NK cells are part of the **innate immune system**. They do not require previous antigen exposure, clonal expansion, or memory formation for their primary activation, allowing for a rapid first-line response. **High-Yield Clinical Pearls for NEET-PG:** * **Surface Markers:** NK cells are characteristically **CD56+** and **CD16+** (the FcγRIII receptor used for Antibody-Dependent Cellular Cytotoxicity - ADCC). They are **CD3 negative**. * **Cytokine Activation:** Their activity is significantly enhanced by **IL-2, IL-12, and Interferon-α/β**. * **Chediak-Higashi Syndrome:** A classic immunodeficiency where NK cell function is impaired due to defective vesicle trafficking.

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Immunology — MCQs

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