Immunology — MCQs
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"HOT SPOT" is the region of an antibody which is also called what?
What is the most common immunoglobulin deficiency?
A mother and newborn are exposed to a pathogen while at the hospital for a routine checkup and breastfeeding clinic. This same pathogen had infected the mother about a year previously, and she had successfully recovered from the subsequent illness. Immunity may be innate or acquired. Which of the following best describes acquired immunity with respect to the newborn?
Burkitt's lymphoma is a malignancy of which type of cells?
Serum sickness is which type of hypersensitivity reaction?
Which of the following acts as an opsonin?
Which of the following statements regarding immunoglobulins is true?
Which one of the following does NOT present antigens?
What type of grafts are transplanted between genetically different members of the same species?
Which of the following is a potent chemotactic factor?
Immunology Indian Medical PG Practice Questions and MCQs
Question 231: "HOT SPOT" is the region of an antibody which is also called what?
- A. Hinge portion
- B. Hypervariable region (Correct Answer)
- C. Constant region
- D. Disulphide bond rich region
Explanation: ### Explanation **Correct Answer: B. Hypervariable region** **Why it is correct:** The **Hypervariable regions** (HVRs) are small segments within the Variable (V) domains of both the heavy and light chains of an antibody. These regions show the highest degree of amino acid sequence variation. Because these specific areas form the actual antigen-binding site (the **Paratope**) and are the points of maximum contact with the antigen, they are colloquially termed **"Hot Spots."** There are three HVRs in each chain, also known as **Complementarity Determining Regions (CDR1, CDR2, and CDR3)**. **Why the other options are incorrect:** * **A. Hinge portion:** This is the flexible segment of the heavy chain (between CH1 and CH2 domains) that allows the antibody arms to move. It is rich in proline and cysteine but does not bind antigens. * **C. Constant region:** This region (CH and CL) determines the biological effector functions (e.g., complement fixation, placental transfer) and the isotype (IgG, IgM, etc.) of the antibody. It does not vary between antibodies of the same class. * **D. Disulphide bond rich region:** While antibodies are held together by interchain and intrachain disulphide bonds, this is a structural feature and not the site of antigen specificity. **High-Yield Facts for NEET-PG:** * **CDR3** is the most variable of the three hypervariable regions and plays the most crucial role in antigen specificity. * **Framework Regions (FRs):** The less variable sequences within the variable domain that support the HVRs. * **Papain digestion** cleaves the antibody *above* the hinge region, resulting in two Fab fragments and one Fc fragment. * **Pepsin digestion** cleaves *below* the hinge region, resulting in one F(ab')2 fragment and degraded Fc fragments.
Question 232: What is the most common immunoglobulin deficiency?
- A. IgA (Correct Answer)
- B. IgE
- C. IgG
- D. IgD
Explanation: **Explanation:** **Selective IgA Deficiency** is the most common primary immunodeficiency disorder worldwide, with an estimated prevalence of approximately 1 in 500 to 1 in 700 individuals in Western populations. **Why IgA is the correct answer:** The deficiency is characterized by serum IgA levels < 7 mg/dL with normal levels of IgG and IgM. It occurs due to a failure in the terminal differentiation of B-cells into IgA-secreting plasma cells. Most patients are asymptomatic, but those who do present clinically often suffer from recurrent sinopulmonary infections, gastrointestinal infections (like Giardiasis), and autoimmune diseases. **Why other options are incorrect:** * **IgE:** Isolated IgE deficiency is rare and clinically insignificant. Conversely, *Hyper-IgE Syndrome (Job Syndrome)* is a distinct, rare primary immunodeficiency. * **IgG:** While IgG subclass deficiencies exist, they are significantly less common than IgA deficiency. A total lack of IgG is usually seen in *X-linked Agammaglobulinemia (Bruton’s)* or *CVID*, which are rarer conditions. * **IgD:** IgD functions primarily as a B-cell surface receptor; an isolated deficiency is not a recognized clinical entity in standard immunodeficiency classifications. **High-Yield Clinical Pearls for NEET-PG:** * **Anaphylaxis Risk:** Patients with IgA deficiency are at high risk of **anaphylaxis during blood transfusions** because they develop anti-IgA antibodies. * **Association:** Strongly associated with **Celiac disease** and **Giardiasis**. * **False Positives:** Can cause false-negative results in Celiac screening tests that rely on IgA anti-tissue transglutaminase (tTG). * **Treatment:** Routine replacement with IVIG is **contraindicated** due to the risk of anaphylaxis.
Question 233: A mother and newborn are exposed to a pathogen while at the hospital for a routine checkup and breastfeeding clinic. This same pathogen had infected the mother about a year previously, and she had successfully recovered from the subsequent illness. Immunity may be innate or acquired. Which of the following best describes acquired immunity with respect to the newborn?
- A. Complement cascade
- B. Increase in C-reactive protein (CRP)
- C. Inflammatory response
- D. Maternal transfer of antibody (Correct Answer)
Explanation: ### Explanation **Correct Option: D. Maternal transfer of antibody** The scenario describes **Naturally Acquired Passive Immunity**. Because the mother was infected a year ago, her immune system developed specific memory B-cells and high titers of **IgG antibodies**. During pregnancy, these IgG antibodies cross the placenta (the only immunoglobulin to do so). Furthermore, since the mother is breastfeeding, she provides **Secretory IgA** to the newborn. These pre-formed antibodies provide immediate, specific protection to the infant against the pathogen they were both exposed to. **Why Incorrect Options are Wrong:** * **A, B, and C (Complement, CRP, and Inflammation):** These are all components of **Innate Immunity**. Innate immunity is non-specific, present from birth, and does not require prior exposure to a pathogen. While they are active in the newborn, they do not represent "acquired" immunity derived from the mother’s previous infection. Specifically, CRP is an acute-phase reactant, and the complement cascade is a biochemical pathway that enhances the ability of antibodies and phagocytes to clear microbes. **High-Yield Clinical Pearls for NEET-PG:** * **Passive Immunity:** Immediate protection but short-lived (no memory). Examples: Placental transfer of IgG, Breast milk (IgA), and administration of Tetanus Immunoglobulin (TIG). * **Active Immunity:** Delayed onset but long-lasting (memory cells). Examples: Natural infection or Vaccination. * **IgG:** The only antibody that crosses the placenta (Neonatal immunity). * **IgA:** The predominant antibody in colostrum and breast milk (Mucosal immunity). * **Mnemonic:** **P**assive = **P**re-formed antibodies; **A**ctive = **A**ntigen exposure.
Question 234: Burkitt's lymphoma is a malignancy of which type of cells?
- A. B cells (Correct Answer)
- B. T cells
- C. Antigen presenting cells
- D. Null cells
Explanation: **Explanation:** **Burkitt’s Lymphoma** is a highly aggressive non-Hodgkin lymphoma (NHL) characterized by the rapid proliferation of **B cells**, specifically those originating from the germinal centers. **Why B cells are the correct answer:** The malignancy is fundamentally a B-cell neoplasm. It is cytogenetically defined by the translocation of the **c-myc proto-oncogene** from chromosome 8 to the immunoglobulin heavy chain locus on **chromosome 14 [t(8;14)]**, or less commonly to the light chain loci on chromosomes 2 or 22. This translocation leads to the constitutive expression of MYC, driving uncontrolled B-cell proliferation. Morphologically, these cells express B-cell markers such as **CD19, CD20, and CD10**. **Why other options are incorrect:** * **T cells:** While T-cell lymphomas exist (e.g., Mycosis fungoides, Adult T-cell leukemia), Burkitt’s is strictly a B-cell malignancy. * **Antigen Presenting Cells (APCs):** These include dendritic cells and macrophages. While B cells can act as APCs, the malignancy arises from the B-cell lineage itself, not from professional phagocytic APCs. * **Null cells:** These are lymphocytes that lack surface markers of either B or T cells (e.g., Natural Killer cells). Burkitt’s cells clearly express B-cell surface immunoglobulins. **High-Yield Clinical Pearls for NEET-PG:** * **Histology:** Classic **"Starry sky" appearance** (tingible body macrophages containing apoptotic debris against a background of dark malignant B cells). * **Association:** Strongly associated with **Epstein-Barr Virus (EBV)**, especially the endemic (African) variant involving the jaw. * **Variants:** Endemic (jaw involvement), Sporadic (abdominal/ileocecal involvement), and Immunodeficiency-associated (HIV). * **Growth Fraction:** One of the highest proliferation rates in human tumors (Ki-67 index near 100%).
Question 235: Serum sickness is which type of hypersensitivity reaction?
- A. Type I
- B. Type II
- C. Type III (Correct Answer)
- D. Type IV
Explanation: **Explanation:** **Serum sickness** is a classic example of **Type III Hypersensitivity**, also known as **Immune Complex-mediated hypersensitivity**. The reaction occurs when an excess of soluble antigens (originally from foreign horse serum, now more commonly from drugs like penicillin or monoclonal antibodies) enters the bloodstream. These antigens bind to specific IgG or IgM antibodies, forming **circulating immune complexes**. Because these complexes are small and formed in antigen excess, they are not easily cleared by the reticuloendothelial system. Instead, they deposit in small blood vessel walls (vasculitis), joints (arthritis), and renal glomeruli (nephritis). This deposition activates the **classical complement pathway**, leading to the recruitment of neutrophils and subsequent tissue damage. **Why other options are incorrect:** * **Type I (Immediate):** Mediated by IgE and mast cell degranulation (e.g., Anaphylaxis, Asthma). * **Type II (Cytotoxic):** Antibodies (IgG/IgM) bind to antigens on *cell surfaces* or tissues, leading to direct cell lysis (e.g., Rh incompatibility, Myasthenia Gravis). * **Type IV (Delayed):** T-cell mediated, involving sensitized T-lymphocytes rather than antibodies (e.g., Mantoux test, Contact dermatitis). **NEET-PG High-Yield Pearls:** * **Clinical Triad:** Fever, Rash (urticarial), and Polyarthralgia. * **Timeline:** Typically occurs 7–14 days after exposure. * **Lab Findings:** Characterized by **low serum complement levels** (C3, C4) due to consumption. * **Arthus Reaction:** This is the *localized* version of Type III hypersensitivity, whereas Serum Sickness is the *systemic* version.
Question 236: Which of the following acts as an opsonin?
- A. C3a
- B. C3b (Correct Answer)
- C. C5a
- D. LTB4
Explanation: **Explanation:** **Opsonization** is the process by which foreign particles (like bacteria) are coated with specific molecules called **opsonins**, making them more "palatable" and easily recognized by phagocytes (neutrophils and macrophages). **Why C3b is the correct answer:** C3b is the most potent opsonin produced by the complement system. When the complement cascade is activated, C3 is cleaved into C3a and C3b. C3b binds covalently to the surface of pathogens. Phagocytes possess specific **CR1 receptors** that bind to C3b, facilitating the attachment and subsequent engulfment of the pathogen. **Analysis of Incorrect Options:** * **C3a and C5a:** These are **Anaphylatoxins**. They trigger mast cell degranulation, leading to histamine release, increased vascular permeability, and smooth muscle contraction. * **C5a and LTB4 (Leukotriene B4):** These are potent **Chemotactic factors**. They act as chemical signals that recruit and attract neutrophils and other inflammatory cells to the site of infection, but they do not coat the pathogen for phagocytosis. **NEET-PG High-Yield Pearls:** 1. **Major Opsonins:** The two most important opsonins in the body are **C3b** (complement-derived) and **IgG** (specifically the Fc portion of IgG1 and IgG3). 2. **Other Opsonins:** Include IgM (indirectly via complement), C4b, Mannose-binding lectin (MBL), and C-reactive protein (CRP). 3. **Mnemonic for Chemotaxis:** "B-A-C-E" (LT**B**4, **A**rachidonic acid metabolites, **C**5a, **E**ndotoxins/Exotoxins). 4. **Deficiency:** Deficiency of C3 leads to recurrent infections with pyogenic bacteria due to impaired opsonization.
Question 237: Which of the following statements regarding immunoglobulins is true?
- A. IgA crosses the placenta.
- B. The half-life of IgG is 23 days. (Correct Answer)
- C. IgD is heat stable.
- D. IgE has the highest carbohydrate content.
Explanation: This question tests the fundamental structural and functional properties of immunoglobulins, a high-yield topic for NEET-PG. **Correct Option Explanation:** **Option B** is correct. **IgG** has the longest half-life of all immunoglobulins, averaging **23 days** (except for the IgG3 subclass, which is ~7 days). This longevity is due to its interaction with the **neonatal Fc receptor (FcRn)**, which protects IgG from lysosomal degradation by recycling it back into the circulation. **Analysis of Incorrect Options:** * **A. IgA crosses the placenta:** Incorrect. **IgG** is the **only** immunoglobulin class capable of crossing the placenta, providing passive immunity to the fetus. * **C. IgD is heat stable:** Incorrect. IgD is highly **heat-labile** and susceptible to proteolytic enzymes. It primarily serves as a surface receptor on B-cells. * **D. IgE has the highest carbohydrate content:** Incorrect. **IgD** has the highest carbohydrate content (~13%). IgE also has high carbohydrate content (~12%), but IgD is the standard answer for the "highest" in this category. **High-Yield Clinical Pearls for NEET-PG:** * **IgG:** Most abundant in serum (80%); responsible for the secondary immune response. * **IgM:** Largest (Pentamer); first to appear in primary response; best at complement fixation. * **IgA:** Found in secretions (tears, saliva, colostrum) as a dimer with a **J-chain** and **secretory component**. * **IgE:** Mediates Type I hypersensitivity and provides defense against helminthic infections. * **Order of serum concentration:** G > A > M > D > E (**GAMDE**).
Question 238: Which one of the following does NOT present antigens?
- A. Natural killer cells (Correct Answer)
- B. Dendritic cells
- C. Langerhan's cells
- D. Macrophages
Explanation: ### Explanation The core concept tested here is the identification of **Antigen-Presenting Cells (APCs)**. APCs are specialized immune cells that capture antigens, process them into peptides, and present them on their surface via **MHC Class II molecules** to T-helper (CD4+) cells to initiate an adaptive immune response. **1. Why Natural Killer (NK) Cells are the Correct Answer:** NK cells are part of the **innate immune system**. Their primary function is to provide a rapid response to virally infected cells and tumor cells by inducing apoptosis through the release of perforins and granzymes. They do **not** possess MHC Class II molecules and do not present antigens to T-cells. Instead, they recognize the "absence of self" (downregulation of MHC Class I) on target cells. **2. Analysis of Incorrect Options (Professional APCs):** * **Dendritic Cells (Option B):** These are the most potent and efficient "professional" APCs. They are the only cells capable of activating naive T-cells. * **Langerhans Cells (Option C):** These are specialized dendritic cells found in the **stratum spinosum** of the epidermis. They capture skin antigens and migrate to local lymph nodes to present them. * **Macrophages (Option D):** These are professional APCs that phagocytose pathogens and present antigens to effector T-cells at the site of infection to enhance the inflammatory response. **Clinical Pearls & High-Yield Facts for NEET-PG:** * **Professional APCs:** Dendritic cells, Macrophages, and B-lymphocytes. * **MHC Requirement:** Professional APCs express **MHC Class II**, whereas almost all nucleated cells express MHC Class I. * **Follicular Dendritic Cells:** Unlike regular dendritic cells, these are found in B-cell follicles and present *unprocessed* antigens to B-cells; they do not express MHC Class II. * **NK Cell Marker:** CD56 and CD16 are the characteristic surface markers for NK cells.
Question 239: What type of grafts are transplanted between genetically different members of the same species?
- A. Autologous grafts
- B. Syngeneic grafts
- C. Allogeneic grafts (Correct Answer)
- D. Xenogeneic grafts
Explanation: **Explanation:** The classification of transplants is based on the genetic relationship between the donor and the recipient. This is a fundamental concept in transplant immunology, specifically concerning **Major Histocompatibility Complex (MHC)** compatibility. **Correct Option: C. Allogeneic grafts (Allografts)** An allograft is a transplant between **genetically non-identical members of the same species** (e.g., human to human). These are the most common types of transplants in clinical practice. Because the donor and recipient have different Human Leukocyte Antigens (HLA), these grafts are prone to rejection and usually require immunosuppressive therapy. **Analysis of Incorrect Options:** * **A. Autologous grafts (Autografts):** Tissue is moved from one site to another on the **same individual** (e.g., skin graft from thigh to arm). There is no risk of rejection. * **B. Syngeneic grafts (Isografts):** Transplants between **genetically identical individuals**, such as monozygotic (identical) twins. Like autografts, these do not trigger an immune response. * **D. Xenogeneic grafts (Xenografts):** Transplants between **different species** (e.g., a porcine/pig heart valve transplanted into a human). These carry the highest risk of hyperacute rejection. **NEET-PG High-Yield Pearls:** * **Order of Rejection Risk:** Autograft = Isograft < Allograft < Xenograft. * **MHC/HLA:** The primary target of the immune response in allografts is the **MHC Molecule** (HLA in humans). * **Graft-versus-Host Disease (GVHD):** Most commonly seen in **Bone Marrow Transplants**, where the immunocompetent donor T-cells attack the recipient's tissues. * **Hyperacute Rejection:** Occurs within minutes due to pre-formed antibodies; it is a Type II Hypersensitivity reaction.
Question 240: Which of the following is a potent chemotactic factor?
- A. C2a
- B. C3b
- C. C4a
- D. C5a (Correct Answer)
Explanation: **Explanation:** The complement system is a crucial component of innate immunity, consisting of proteins that enhance the ability of antibodies and phagocytic cells to clear pathogens. **Correct Option: D (C5a)** C5a is the most potent **anaphylatoxin** and **chemotactic factor** of the complement system. It acts as a powerful chemoattractant for neutrophils, eosinophils, monocytes, and macrophages. By binding to specific receptors on these cells, C5a triggers their migration to the site of inflammation, promotes degranulation of mast cells (releasing histamine), and increases vascular permeability. **Incorrect Options:** * **A (C2a):** This is a fragment of C2. While it contributes to the formation of C3 convertase (C4b2a), it does not possess significant chemotactic properties. * **B (C3b):** This is the primary **opsonin** of the complement system. Its main function is "opsonization"—coating bacteria to make them more easily recognized and engulfed by phagocytes (via CR1 receptors). * **C (C4a):** This is a weak anaphylatoxin. While it can cause some smooth muscle contraction and vascular permeability, its potency is significantly lower than C5a and it is not a major chemotactic agent. **High-Yield Clinical Pearls for NEET-PG:** * **Chemotactic Hierarchy:** C5a > LTB4 > IL-8 > Bacterial products (N-formyl peptides). * **Opsonization:** C3b and IgG are the two most important opsonins. * **Membrane Attack Complex (MAC):** Formed by C5b-C9; responsible for cell lysis. * **Anaphylatoxins:** C5a > C3a > C4a (in order of potency). * **Deficiency:** C5-C9 deficiency increases susceptibility to *Neisseria* infections.
Practice by Chapter
Cells and Organs of Immune System
Practice Questions
Innate Immunity
Practice Questions
Adaptive Immunity
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Antigens and Antibodies
Practice Questions
Major Histocompatibility Complex
Practice Questions
Complement System
Practice Questions
Cytokines and Chemokines
Practice Questions
Hypersensitivity Reactions
Practice Questions
Autoimmunity and Autoimmune Diseases
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Immunodeficiency Disorders
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Transplantation Immunology
Practice Questions
Tumor Immunology
Practice Questions
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