Immunology — MCQs
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One of the most remarkable aspects of the human immune system is its diversity, that is, the ability to recognize a wide range of antigens and to mount a specific antibody response. This is called clonal selection. At the cellular level, which of the following are primarily responsible for such specificity?
A 9-year-old girl receives an intradermal tuberculin injection and later develops an indurated, erythematous papule 12 mm in diameter. This reaction is an example of which of the following?
Which antibody is the most avidly complement fixing?
What is the marker for NK cell activity?
Mixed lymphocyte culture is used to identify which of the following?
During an infection with Streptococcus pyogenes, an individual generated sufficiently high levels of IgM and IgG antibodies against Streptococcus pyogenes antigen with structural similarities to the heart, causing cardiac damage. In this example, what process explains how the microbe contributed to autoimmunity?
Both B and T cell defect is present in all EXCEPT:
The Nitroblue Tetrazolium Test is used for assessing which process?
Which of the following is NOT a true statement regarding Natural Killer (NK) cells?
Which of the following is true about immunoglobulin gene rearrangement and immunoglobulin diversity?
Immunology Indian Medical PG Practice Questions and MCQs
Question 351: One of the most remarkable aspects of the human immune system is its diversity, that is, the ability to recognize a wide range of antigens and to mount a specific antibody response. This is called clonal selection. At the cellular level, which of the following are primarily responsible for such specificity?
- A. Cytotoxic T cells
- B. Hypervariable regions in domains of B cells (Correct Answer)
- C. The major histocompatibility complex
- D. Specific T cell receptors
Explanation: The core of the immune system's diversity lies in its ability to generate millions of unique antigen-binding sites. This specificity is primarily driven by the **Hypervariable regions** (also known as Complementarity Determining Regions or CDRs) located within the variable domains of B cell receptors (immunoglobulins). ### Why the Correct Answer is Right The **Hypervariable regions** are three small loops (CDR1, CDR2, and CDR3) on both the light and heavy chains of the B cell receptor. These regions undergo extensive genetic recombination (V(D)J recombination) and somatic hypermutation. Because these loops form the actual contact surface with the antigen (the paratope), their extreme structural diversity allows the B cell pool to recognize a virtually limitless array of epitopes. This is the structural basis for the **Clonal Selection Theory**, where a specific antigen "selects" the B cell with the matching hypervariable region to proliferate. ### Why Other Options are Incorrect * **Cytotoxic T cells (A):** These are effector cells responsible for killing virally infected or tumor cells; they do not produce antibodies. * **Major Histocompatibility Complex (C):** MHC molecules are involved in antigen *presentation* (MHC I to CD8+ and MHC II to CD4+ cells), not the primary generation of antibody diversity. * **Specific T cell receptors (D):** While TCRs are specific, the question specifically asks about the mounting of an **antibody response**, which is a function unique to B cells and their differentiated plasma cells. ### NEET-PG High-Yield Pearls * **CDR3** is the most variable of the three hypervariable regions and plays the most crucial role in antigen binding. * **Somatic Hypermutation:** Occurs in the germinal centers of lymph nodes, further refining the affinity of hypervariable regions after antigen exposure (Affinity Maturation). * **Clonal Selection:** Proposed by Macfarlane Burnet; it states that one B cell clone expresses only one type of receptor specificity.
Question 352: A 9-year-old girl receives an intradermal tuberculin injection and later develops an indurated, erythematous papule 12 mm in diameter. This reaction is an example of which of the following?
- A. Antibody-dependent cell-mediated cytotoxicity
- B. Local anaphylaxis
- C. T-cell mediated cytotoxicity
- D. Type IV hypersensitivity (Correct Answer)
Explanation: ### Explanation **Correct Option: D. Type IV hypersensitivity** The clinical scenario describes a classic **Mantoux (Tuberculin) test** reaction. Type IV hypersensitivity, also known as **Delayed-Type Hypersensitivity (DTH)**, is mediated by T-lymphocytes rather than antibodies. Upon intradermal injection of PPD (Purified Protein Derivative), sensitized **Th1 cells** release cytokines (IFN-γ, IL-2), which recruit and activate macrophages. This process takes **48–72 hours** to manifest as the indurated papule described. **Analysis of Incorrect Options:** * **A. Antibody-dependent cell-mediated cytotoxicity (ADCC):** This is a mechanism associated with **Type II hypersensitivity**, where NK cells or macrophages kill target cells coated with IgG antibodies (e.g., transplant rejection). * **B. Local anaphylaxis:** This refers to **Type I hypersensitivity**, which is IgE-mediated and occurs within minutes (immediate) due to mast cell degranulation. * **C. T-cell mediated cytotoxicity:** While also a form of Type IV hypersensitivity, this specifically involves **CD8+ T-cells** directly killing target cells (e.g., viral infections or contact dermatitis). The tuberculin reaction is primarily a **CD4+ Th1-mediated** inflammatory response. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Hypersensitivity (Gell & Coombs):** **A**cid (Type I: **A**llergic/Anaphylactic), **C**ytotoxic (Type II), **I**mmune-Complex (Type III), **D**elayed (Type IV). * **Type IV Examples:** Mantoux test, Contact dermatitis (Nickel, Poison Ivy), Lepromin test, and Granuloma formation (Tuberculosis, Sarcoidosis). * **Key Cells:** The hallmark of Type IV is the absence of antibodies; it is entirely **cell-mediated**. * **Induration vs. Erythema:** In a Mantoux test, only the **induration** (palpable hardness) is measured, not the erythema (redness).
Question 353: Which antibody is the most avidly complement fixing?
- A. IgA
- B. IgG (Correct Answer)
- C. IgM
- D. IgE
Explanation: **Explanation:** The ability of an antibody to fix complement via the **Classical Pathway** depends on its structure and the availability of binding sites for the **C1q** molecule. **Why IgG is the correct answer:** While a single molecule of IgM is technically more efficient at initiating the complement cascade due to its pentameric structure, **IgG** is considered the most significant complement-fixing antibody in the context of standard medical examinations like NEET-PG when discussing overall serum activity and clinical relevance. Specifically, **IgG3** is the most potent subclass, followed by IgG1 and IgG2. IgG fixes complement after binding to an antigen, which causes a conformational change in its Fc region, allowing C1q to bind. **Analysis of Incorrect Options:** * **IgM:** Often causes confusion because it is the *most efficient* on a per-molecule basis (only one pentamer is needed). However, in many textbook contexts, IgG is highlighted for its dominant role in systemic complement activation. (Note: If the question asks for the "most efficient" or "first" antibody, IgM is the choice; for "most avidly/clinically significant," IgG is often the keyed answer). * **IgA:** Primarily functions in mucosal immunity. It does not activate the classical pathway; it can only weakly activate the **alternative pathway**. * **IgE:** Involved in Type I hypersensitivity and parasitic infections. It does not fix complement. **NEET-PG High-Yield Pearls:** 1. **Order of Complement Fixation (IgG subclasses):** IgG3 > IgG1 > IgG2. (IgG4 does *not* fix complement). 2. **Pathway Trigger:** The Classical pathway is triggered by **Antigen-Antibody complexes** (IgG or IgM). 3. **C3:** This is the most abundant complement component in the serum and the point where all three pathways (Classical, Alternative, Lectin) converge.
Question 354: What is the marker for NK cell activity?
- A. CD3
- B. CD4
- C. CD56 (Correct Answer)
- D. CD19
Explanation: **Explanation:** Natural Killer (NK) cells are large granular lymphocytes that play a critical role in the innate immune system by providing a first-line defense against virally infected cells and tumor cells. **Why CD56 is the correct answer:** CD56 (Neural Cell Adhesion Molecule or NCAM) is the definitive phenotypic marker used to identify NK cells in clinical practice and flow cytometry. While NK cells are also characterized by the expression of **CD16** (an Fc receptor for IgG that mediates Antibody-Dependent Cellular Cytotoxicity or ADCC), **CD56** is the most widely used marker for their identification. NK cells are uniquely defined as being **CD3 negative** and **CD56 positive**. **Analysis of Incorrect Options:** * **CD3:** This is the pan-T cell marker. It is part of the T-cell receptor (TCR) complex. Its absence is a key feature used to distinguish NK cells from T-lymphocytes. * **CD4:** This is a marker for Helper T-cells (Th cells) and is also found on monocytes and dendritic cells. It interacts with MHC class II molecules. * **CD19:** This is a primary marker for B-cells (along with CD20 and CD21). It is involved in B-cell signaling and activation. **High-Yield Clinical Pearls for NEET-PG:** * **NK Cell Function:** They do not require prior sensitization and lack antigen-specific receptors. They kill cells that show "missing self" (downregulation of MHC-I). * **Markers:** NK cells are **CD3–, CD16+, and CD56+**. * **Cytokine Activation:** NK cell activity is significantly enhanced by **IL-2 and IL-12**. * **LAK Cells:** NK cells treated with high doses of IL-2 become Lymphokine-Activated Killer (LAK) cells, used in experimental cancer immunotherapy.
Question 355: Mixed lymphocyte culture is used to identify which of the following?
- A. MHC class I antigen
- B. MHC class II antigen (Correct Answer)
- C. B lymphocytes
- D. T helper cells
Explanation: **Explanation:** **Mixed Lymphocyte Reaction (MLR)**, also known as Mixed Lymphocyte Culture, is a functional assay used to determine the degree of histocompatibility between a donor and a recipient. 1. **Why MHC Class II is correct:** The MLR primarily detects differences in **MHC Class II (HLA-D)** antigens. When lymphocytes from two different individuals are cultured together, the T-cells of one individual recognize the foreign MHC Class II molecules on the surface of the other individual's cells (specifically on B-cells or monocytes). This recognition triggers T-cell activation and proliferation. The degree of proliferation is proportional to the disparity in MHC Class II antigens. 2. **Why other options are incorrect:** * **MHC Class I:** These are typically identified using **Serological methods** (Lymphocytotoxicity tests) rather than culture-based proliferation assays. * **B lymphocytes & T helper cells:** While these cells are *participants* in the reaction (B-cells act as stimulators and T-cells as responders), the test is designed to identify the **antigenic compatibility** of the tissue, not to quantify or identify the cell types themselves. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Use:** MLR was traditionally the "gold standard" for predicting **Graft-versus-Host Disease (GVHD)** in bone marrow transplants. * **One-way vs. Two-way MLR:** In clinical practice, a "one-way" MLR is used where the donor cells are irradiated (treated with Mitomycin C) so they cannot divide, allowing only the recipient's T-cell response to be measured. * **Modern Alternative:** MLR has largely been replaced by rapid **PCR-based DNA sequencing** for HLA typing, but it remains a classic exam topic for understanding cellular immunity.
Question 356: During an infection with Streptococcus pyogenes, an individual generated sufficiently high levels of IgM and IgG antibodies against Streptococcus pyogenes antigen with structural similarities to the heart, causing cardiac damage. In this example, what process explains how the microbe contributed to autoimmunity?
- A. Anergy
- B. Central tolerance
- C. Epitope spreading
- D. Molecular mimicry (Correct Answer)
Explanation: ### Explanation **1. Why Molecular Mimicry is Correct:** Molecular mimicry occurs when a foreign antigen shares structural similarities (sequence or conformational) with self-antigens. In the case of *Streptococcus pyogenes* (Group A Strep), the **M protein** in the bacterial cell wall is structurally similar to **myosin** in the human heart and proteins in the joints and brain. The immune system, while attempting to eliminate the bacteria, produces antibodies (IgM and IgG) that cross-react with these self-tissues. This is the classic pathophysiological mechanism behind **Acute Rheumatic Fever (ARF)**. **2. Why Other Options are Incorrect:** * **Anergy:** This refers to a state of immune unresponsiveness where T or B cells become functionally inactive after encountering an antigen without necessary co-stimulatory signals. It is a mechanism of peripheral tolerance, not a cause of autoimmunity. * **Central Tolerance:** This occurs during lymphocyte development in the thymus (T cells) or bone marrow (B cells), where self-reactive clones are deleted (negative selection). Failure of this leads to autoimmunity, but it is not triggered by microbial similarity. * **Epitope Spreading:** This is a process where an initial immune response against one epitope evolves to include responses against other, non-cross-reacting epitopes on the same or different proteins. While it can perpetuate autoimmune disease, it is not the initial "trigger" described in this scenario. **3. Clinical Pearls for NEET-PG:** * **Classic Example:** *S. pyogenes* M protein vs. Cardiac Myosin (Rheumatic Heart Disease). * **Other Examples:** *Campylobacter jejuni* lipooligosaccharides vs. Gangliosides (Guillain-Barré Syndrome). * **Type of Hypersensitivity:** Acute Rheumatic Fever is a **Type II Hypersensitivity** reaction. * **Jones Criteria:** Remember this for the clinical diagnosis of Rheumatic Fever (Joints, Carditis, Nodules, Erythema marginatum, Sydenham chorea).
Question 357: Both B and T cell defect is present in all EXCEPT:
- A. Severe combined immunodeficiency (SCID)
- B. Common variable immunodeficiency (CVID)
- C. Wiskott-Aldrich syndrome
- D. X-linked Agammaglobulinemia (Correct Answer)
Explanation: **Explanation:** The core concept tested here is the distinction between **Combined Immunodeficiencies** (affecting both B and T cells) and **Pure B-cell defects**. **Why X-linked Agammaglobulinemia (XLA) is the correct answer:** XLA (Bruton’s Agammaglobulinemia) is a **pure B-cell deficiency**. It is caused by a mutation in the **BTK (Bruton Tyrosine Kinase) gene**, which is essential for B-cell maturation. In XLA, B-cell precursors fail to develop into mature B-cells, leading to a complete absence of B-cells in peripheral blood and very low levels of all immunoglobulin classes. Importantly, **T-cell number and function remain normal.** **Analysis of Incorrect Options:** * **SCID:** As the name suggests, it is a "combined" defect. It involves a total failure of both humoral (B-cell) and cell-mediated (T-cell) immunity due to defects like IL-2 receptor gamma chain deficiency or ADA deficiency. * **Wiskott-Aldrich Syndrome:** This is a triad of eczema, thrombocytopenia, and immunodeficiency. It is a combined immunodeficiency where T-cell function progressively declines, and B-cell responses to polysaccharide antigens are impaired. * **CVID:** While primarily characterized by hypogammaglobulinemia, most patients also exhibit significant **T-cell dysfunction** (e.g., reduced cytokine production or T-cell exhaustion), classifying it as a defect affecting both arms of the immune system. **High-Yield Clinical Pearls for NEET-PG:** * **XLA:** Look for a male infant (X-linked) with recurrent pyogenic infections (e.g., *S. pneumoniae*, *H. influenzae*) after 6 months of age (once maternal IgG wanes) and **absent tonsils/adenoids**. * **SCID:** A medical emergency; requires Bone Marrow Transplant. Look for "absent thymic shadow" on X-ray. * **Wiskott-Aldrich:** Remember the mnemonic **WAITER**: **W**iskott-**A**ldrich, **I**mmunodeficiency, **T**hrombocytopenia, **E**czema, **R**ecurrent infections. High risk of Non-Hodgkin Lymphoma.
Question 358: The Nitroblue Tetrazolium Test is used for assessing which process?
- A. Phagocytosis (Correct Answer)
- B. Complement activation
- C. T cell function
- D. B cell proliferation
Explanation: **Explanation:** The **Nitroblue Tetrazolium (NBT) Test** is a classic diagnostic tool used to evaluate the **metabolic burst (oxidative burst)** activity of phagocytic cells, specifically neutrophils. 1. **Why Phagocytosis is Correct:** During phagocytosis, neutrophils produce reactive oxygen species (ROS) like superoxide radicals via the enzyme **NADPH oxidase**. In the NBT test, the colorless NBT dye is added to a sample of the patient's blood. If the phagocytes are functioning correctly, the superoxide radicals reduce the yellow NBT dye into insoluble, dark blue **formazan crystals**. A positive test (blue color) indicates normal oxidative killing, while a negative test (no color change) indicates a defect in this process. 2. **Why Other Options are Incorrect:** * **Complement activation:** Assessed by tests like CH50 (classical pathway) or AH50 (alternative pathway). * **T cell function:** Evaluated via Skin Delayed-Type Hypersensitivity (DTH) tests or Flow Cytometry (CD3/CD4/CD8 counts). * **B cell proliferation:** Assessed by measuring serum immunoglobulin levels or using Mitogen stimulation tests. **High-Yield Clinical Pearls for NEET-PG:** * **Chronic Granulomatous Disease (CGD):** This is the primary condition diagnosed using the NBT test. It is characterized by a deficiency in **NADPH oxidase**, leading to recurrent infections with **catalase-positive organisms** (e.g., *S. aureus*, *Aspergillus*, *Serratia*). * **Modern Alternative:** The **Dihydrorhodamine (DHR) 123 flow cytometry test** is now the preferred "gold standard" over NBT due to its higher sensitivity and quantitative nature. * **Inheritance:** CGD is most commonly **X-linked recessive**.
Question 359: Which of the following is NOT a true statement regarding Natural Killer (NK) cells?
- A. NK cells have a significant role in cell-mediated immunity. (Correct Answer)
- B. NK cells are part of the innate immune system.
- C. NK cells are typically CD16 positive.
- D. NK cells are typically CD56 positive.
Explanation: **Explanation:** The core concept tested here is the classification of immune cells. While **Natural Killer (NK) cells** are lymphocytes, they are fundamentally part of the **innate immune system**, not the adaptive (acquired) immune system. 1. **Why Option A is the Correct Answer (The False Statement):** "Cell-mediated immunity" (CMI) specifically refers to the adaptive immune response mediated by **T-lymphocytes** (T-helper and Cytotoxic T-cells). CMI is characterized by antigen specificity and memory. NK cells, conversely, do not possess T-cell receptors (TCR) or undergo gene rearrangement; they provide a non-specific, rapid first line of defense without requiring prior sensitization. Therefore, they are not considered primary mediators of CMI. 2. **Analysis of Incorrect Options (True Statements):** * **Option B:** NK cells are indeed part of the **innate immune system**. They recognize "stressed" cells (virally infected or tumor cells) that have downregulated MHC Class I molecules (the "missing self" hypothesis). * **Option C & D:** These are the definitive phenotypic markers for NK cells. **CD56** (NCAM) is the universal marker used to identify them, while **CD16** (FcγRIII) allows NK cells to bind to IgG-coated target cells, mediating **Antibody-Dependent Cellular Cytotoxicity (ADCC)**. **High-Yield NEET-PG Pearls:** * **Morphology:** NK cells are identified histologically as **Large Granular Lymphocytes (LGLs)**. * **Cytokines:** Their activity is significantly enhanced by **IL-2, IL-12, and IFN-α/β**. * **Receptors:** They use **KIRs** (Killer Immunoglobulin-like Receptors) to monitor MHC Class I expression on host cells. * **Granules:** They kill targets via **Perforins** (create pores) and **Granzymes** (induce apoptosis).
Question 360: Which of the following is true about immunoglobulin gene rearrangement and immunoglobulin diversity?
- A. Somatic mutations theory (Correct Answer)
- B. One loop and two loop joining theory
- C. DNA rearrangement
- D. Appropriate class switching
Explanation: The generation of antibody diversity is a complex genetic process that allows the human body to produce millions of different immunoglobulins from a limited number of genes. ### **Explanation of the Correct Answer** **A. Somatic Mutation Theory:** This is a primary mechanism for generating immunoglobulin diversity. Specifically, **Somatic Hypermutation** occurs in B cells within the germinal centers of lymph nodes after exposure to an antigen. It involves point mutations in the variable (V) regions of the heavy and light chains. This process leads to **Affinity Maturation**, where B cells with the highest affinity for the antigen are selected to survive, ensuring a more effective immune response. ### **Analysis of Incorrect Options** * **B. One loop and two loop joining theory:** This is not a standard term in immunology. The correct mechanism for joining gene segments is the **12/23 rule** (RSS - Recombination Signal Sequences), which ensures that a V segment joins to a D or J segment correctly. * **C. DNA rearrangement:** While V(D)J recombination *is* a form of DNA rearrangement, the question specifically asks for the theory governing the vast diversity and refinement of antibodies. Somatic mutation is the specific "theory" historically contrasted with the "germline theory" to explain how diversity exceeds what is encoded in the genome. * **D. Appropriate class switching:** Isotype (class) switching changes the constant region of the heavy chain (e.g., IgM to IgG). While it changes the *function* of the antibody, it **does not** change the antigen-binding specificity or contribute to the diversity of the variable region. ### **High-Yield Clinical Pearls for NEET-PG** * **V(D)J Recombination:** Occurs in the bone marrow (antigen-independent). Mediated by **RAG-1 and RAG-2** genes. * **Junctional Diversity:** The most significant contribution to diversity, caused by the addition of P-nucleotides and N-nucleotides (via **TdT enzyme**). * **AID Enzyme:** Activation-induced cytidine deaminase (AID) is essential for both **Somatic Hypermutation** and **Class Switching**. Deficiency leads to Hyper-IgM Syndrome.
Practice by Chapter
Cells and Organs of Immune System
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Innate Immunity
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Adaptive Immunity
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Antigens and Antibodies
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Major Histocompatibility Complex
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Complement System
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Cytokines and Chemokines
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Hypersensitivity Reactions
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Autoimmunity and Autoimmune Diseases
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Immunodeficiency Disorders
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Transplantation Immunology
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Tumor Immunology
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