Immunology — MCQs
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The opsonic index is the ratio of which of the following?
Which of the following is NOT a mononuclear-macrophage?
Which phospholipid is used to investigate syphilis by the reagin test?
Which one of the following is called the immunologically sequestered antigen?
Which complex of the complement system is known as the Membrane Attack Complex (MAC)?
AB blood group antigens are known as which factor?
Which of the following is an example of a Type III hypersensitivity reaction?
In PCR, why is Thermus aquaticus preferred over E. coli?
Which of the following molecular phenomena in Ig genes is responsible for affinity maturation of antibody response?
A 31-year-old male patient complains of fatigue, oral candidiasis, and axillary lymphadenopathy. He reports engaging in high-risk behavior 6 years ago during a trip to eastern and southern Africa. His prior HIV test was reported as negative. Which one of the following diagnostic steps would be most appropriate?
Immunology Indian Medical PG Practice Questions and MCQs
Question 131: The opsonic index is the ratio of which of the following?
- A. C3b opsonin to antibody opsonin
- B. Phagocytic activity of a patient to the phagocytic activity of a normal individual (Correct Answer)
- C. Serum concentration of opsonin in a patient to the serum concentration in a normal individual
- D. Complement activity in a patient to complement activity in a normal individual
Explanation: ### Explanation **1. Why the Correct Answer is Right** The **Opsonic Index** is a quantitative measure used to assess the phagocytic power of a patient’s blood against a specific microorganism. It is defined as the ratio of the number of bacteria phagocytosed by a patient's phagocytes (in the presence of their own serum) to the number of bacteria phagocytosed by a healthy individual's phagocytes (in the presence of normal serum). * **Formula:** Opsonic Index = (Phagocytic activity of patient’s blood) / (Phagocytic activity of normal blood). * **Concept:** Opsonization is the process where "opsonins" (like IgG and C3b) coat an antigen to make it more "palatable" to phagocytes. A higher index indicates a more robust immune response or recovery phase. **2. Why the Other Options are Wrong** * **Option A:** While C3b and antibodies are the two primary opsonins, the index measures the *functional outcome* (phagocytosis), not a ratio between different types of opsonins. * **Option B & D:** The index is a functional assay of cellular activity (phagocytosis), not a direct measurement of the serum concentration of proteins or the total hemolytic complement activity (CH50). **3. Clinical Pearls & High-Yield Facts for NEET-PG** * **Opsonins:** The most important opsonins are **IgG** (specifically IgG1 and IgG3) and **C3b**. * **Mechanism:** Opsonins overcome the negative electrostatic repulsion between the bacterial surface and the host cell membrane. * **Clinical Significance:** The opsonic index was historically used to monitor the progress of chronic infections (like Tuberculosis) and to gauge the effectiveness of vaccines; a rising index usually indicates a favorable prognosis. * **Related Concept:** **Phagocytic Index** refers to the average number of bacteria ingested by a single leucocyte. The Opsonic Index is the ratio of two such Phagocytic Indices.
Question 132: Which of the following is NOT a mononuclear-macrophage?
- A. Histiocytes
- B. Microglia
- C. Kupffer cells
- D. B-cells (Correct Answer)
Explanation: ### Explanation The **Mononuclear Phagocyte System (MPS)**, formerly known as the Reticuloendothelial System, consists of phagocytic cells derived from bone marrow hematopoietic stem cells (monoblasts). These cells circulate in the blood as **monocytes** and eventually migrate into various tissues to mature into specialized **macrophages**. **Why B-cells are the correct answer:** B-cells are **lymphocytes**, not part of the mononuclear-macrophage lineage. While B-cells can function as Professional Antigen-Presenting Cells (APCs), they are primarily responsible for humoral immunity (antibody production) and do not possess the phagocytic morphology or lineage markers of the MPS. **Analysis of incorrect options:** * **Histiocytes:** These are the resident macrophages found in **connective tissue**. * **Microglia:** These are the specialized macrophages of the **Central Nervous System (CNS)**. They are unique as they are the only immune cells resident in the brain parenchyma. * **Kupffer cells:** These are specialized macrophages located in the **liver sinusoids**, responsible for clearing pathogens and aged erythrocytes from the portal circulation. **High-Yield Clinical Pearls for NEET-PG:** * **Other Tissue Macrophages:** * **Alveolar Macrophages:** Dust cells (Lungs) * **Osteoclasts:** Bone * **Mesangial cells:** Kidney * **Langerhans cells:** Skin (Note: These are dendritic cells, but often grouped in older MPS classifications). * **Littoral cells:** Spleen * **Key Marker:** **CD14** is a specific surface marker for monocytes and macrophages. * **Function:** Macrophages are essential for innate immunity, chronic inflammation, and secreting cytokines like IL-1, IL-6, and TNF-α.
Question 133: Which phospholipid is used to investigate syphilis by the reagin test?
- A. Cardiolipin (Correct Answer)
- B. Plasminogen
- C. Palmitoyl lecithin
- D. Serine
Explanation: **Explanation:** The correct answer is **Cardiolipin**. Syphilis, caused by *Treponema pallidum*, triggers the production of two types of antibodies: specific treponemal antibodies and non-specific **reaginic antibodies**. Reaginic antibodies (IgM and IgG) are produced against lipid antigens released from host cells damaged by the infection. The antigen used in non-specific tests (like VDRL and RPR) is **Cardiolipin** (diphosphatidylglycerol), which is chemically extracted from beef heart. To enhance its reactivity and stability in the laboratory, it is fortified with **lecithin** and **cholesterol**. **Analysis of Options:** * **B. Plasminogen:** This is a plasma protein involved in fibrinolysis (clot breakdown) and has no role in syphilis serology. * **C. Palmitoyl lecithin:** While lecithin is a component of the VDRL antigen, it serves as a stabilizing agent rather than the primary reactive phospholipid. * **D. Serine:** This is an amino acid, not a phospholipid. **High-Yield Clinical Pearls for NEET-PG:** * **Reagin Tests:** VDRL (Venereal Disease Research Laboratory) and RPR (Rapid Plasma Reagin) are used for **screening** and monitoring treatment response (titer falls after successful therapy). * **Biological False Positives (BFP):** Since cardiolipin is a host-derived lipid, BFP can occur in conditions like SLE, Leprosy, Malaria, and Pregnancy. * **Prozone Phenomenon:** In secondary syphilis, very high antibody titers can lead to a false-negative result; the serum must be diluted to get a positive reaction.
Question 134: Which one of the following is called the immunologically sequestered antigen?
- A. Lungs
- B. Spleen
- C. Thymus
- D. Lens of the eye (Correct Answer)
Explanation: ### Explanation **Concept: Immunological Privilege and Sequestered Antigens** Immunologically sequestered antigens are self-antigens that are anatomically isolated from the immune system during embryonic development. Because they never come into contact with lymphoid tissues during the period of "self-tolerance" induction, the immune system does not recognize them as "self." If these antigens are later released into circulation due to trauma or infection, the body treats them as foreign, leading to an autoimmune response. **Why the Lens of the Eye is Correct:** The **lens of the eye** is an avascular structure enclosed in a thick capsule. Its proteins (crystallins) are physically separated from the systemic circulation and immune cells. If the lens capsule is ruptured (e.g., during cataract surgery or trauma), these sequestered antigens are exposed, potentially triggering **phacoantigenic uveitis**, an inflammatory autoimmune reaction. **Analysis of Incorrect Options:** * **Lungs:** These are highly vascular organs with constant exposure to systemic circulation and a robust local immune system (Alveolar macrophages, BALT). * **Spleen:** This is a secondary lymphoid organ. It is the primary site for filtering blood-borne antigens and is inherently part of the immune system. * **Thymus:** This is a primary lymphoid organ where T-cell maturation occurs. It is where "central tolerance" is established, not a site of sequestration. **High-Yield Clinical Pearls for NEET-PG:** * **Other Sequestered Sites:** Spermatozoa (testis), Brain (Blood-Brain Barrier), and the Uveal tract. * **Sympathetic Ophthalmitis:** A classic exam example where trauma to one eye releases sequestered uveal antigens, causing the immune system to attack the *uninjured* eye. * **Mechanism:** The primary failure in diseases involving sequestered antigens is a lack of **peripheral tolerance**.
Question 135: Which complex of the complement system is known as the Membrane Attack Complex (MAC)?
- A. C3a
- B. C3b
- C. C5-9 (Correct Answer)
- D. C4b
Explanation: **Explanation:** The complement system is a vital component of innate immunity, consisting of a cascade of proteins that enhance the ability of antibodies and phagocytic cells to clear pathogens. **Why C5-9 is Correct:** The **Membrane Attack Complex (MAC)** is the final common pathway of all three complement activation routes (Classical, Alternative, and Lectin). It is formed by the sequential assembly of complement components **C5b, C6, C7, C8, and multiple C9 molecules**. This complex inserts itself into the lipid bilayer of the target cell membrane, forming a transmembrane pore. This leads to the loss of osmotic integrity, resulting in water influx and subsequent **osmotic lysis** of the pathogen. **Analysis of Incorrect Options:** * **C3a:** This is an **anaphylatoxin**. It triggers mast cell degranulation, leading to increased vascular permeability and smooth muscle contraction. * **C3b:** This is the primary **opsonin** of the complement system. It coats the surface of bacteria, making them more "tasty" for recognition and engulfment by phagocytes (via CR1 receptors). * **C4b:** This is a component of the C3 convertase in the classical and lectin pathways (C4b2a). While it helps propagate the cascade, it does not form the lytic pore. **High-Yield Clinical Pearls for NEET-PG:** * **Deficiency:** Patients with deficiencies in late complement components (**C5 to C9**) have a significantly increased susceptibility to recurrent infections by **Neisseria species** (Meningitidis and Gonorrhoeae). * **Potency:** C5a is the most potent anaphylatoxin and a strong chemoattractant for neutrophils. * **Regulation:** CD59 (Protectin) is a human cell surface protein that inhibits MAC formation, protecting host cells from "bystander" lysis. Its absence is seen in Paroxysmal Nocturnal Hemoglobinuria (PNH).
Question 136: AB blood group antigens are known as which factor?
- A. Duffy
- B. Landsteiner (Correct Answer)
- C. Rhesus
- D. Lutheran
Explanation: ### Explanation **Correct Answer: B. Landsteiner** **Reasoning:** The AB blood group antigens (A and B) are referred to as **Landsteiner factors** because they were discovered by **Karl Landsteiner** in 1900. He identified the ABO blood group system, which is the most important system in transfusion medicine. For this monumental discovery, which laid the foundation for safe blood transfusions, he was awarded the **Nobel Prize in Physiology or Medicine in 1930**. Landsteiner’s Law states that if an agglutinogen (antigen) is present on red blood cells, the corresponding agglutinin (antibody) must be absent from the plasma, and vice versa. **Analysis of Incorrect Options:** * **A. Duffy:** This is a minor blood group system. The Duffy antigen (Fy) acts as a receptor for *Plasmodium vivax*. Individuals who are Duffy-negative (common in African populations) are resistant to *P. vivax* malaria. * **C. Rhesus (Rh):** Discovered later by Landsteiner and Wiener in 1940 (using Rhesus monkeys). While crucial for clinical practice (e.g., Hemolytic Disease of the Newborn), the term "Landsteiner factors" specifically honors his primary discovery of the ABO system. * **D. Lutheran:** Another minor blood group system (Lu) consisting of antigens located on a glycoprotein of the immunoglobulin superfamily. It is rarely involved in severe transfusion reactions. **High-Yield Clinical Pearls for NEET-PG:** * **Universal Donor:** O negative (no A, B, or Rh antigens). * **Universal Recipient:** AB positive (no anti-A, anti-B, or anti-Rh antibodies). * **Bombay Blood Group:** Characterized by the absence of the **H antigen**. These individuals type as 'O' but have anti-H antibodies, making them compatible only with other Bombay group donors. * **Secretors:** Approximately 80% of the population secrete ABO antigens in body fluids (saliva, semen) due to the presence of the **Se gene**.
Question 137: Which of the following is an example of a Type III hypersensitivity reaction?
- A. Pemphigus vulgaris
- B. Myasthenia gravis
- C. Pernicious anemia
- D. Arthus reaction (Correct Answer)
Explanation: **Explanation:** **Type III Hypersensitivity** is an **immune-complex-mediated** reaction. It occurs when soluble antigen-antibody (IgG or IgM) complexes are not adequately cleared, leading to their deposition in tissues (like blood vessel walls, joints, or kidneys). This triggers the classical complement pathway, resulting in neutrophil recruitment and tissue damage. * **Why D is correct:** The **Arthus reaction** is the classic localized example of Type III hypersensitivity. It occurs when an antigen is injected into the skin of an individual with high levels of pre-existing circulating IgG antibodies. This leads to local immune complex formation, vasculitis, and localized tissue necrosis. **Analysis of Incorrect Options:** * **A, B, and C (Pemphigus vulgaris, Myasthenia gravis, Pernicious anemia):** These are all examples of **Type II Hypersensitivity** (Antibody-mediated/Cytotoxic). In Type II, antibodies are directed against **fixed antigens** on specific cell surfaces or tissues, rather than forming soluble circulating complexes. * *Pemphigus:* Antibodies against desmogleins. * *Myasthenia Gravis:* Antibodies against ACh receptors. * *Pernicious Anemia:* Antibodies against intrinsic factor or parietal cells. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Type III:** **S**-**S**-**A**-**P** (Systemic Lupus Erythematosus, Serum Sickness, Arthus Reaction, Post-streptococcal Glomerulonephritis). * **Key Mediator:** Complement (C5a) attracts **Neutrophils**, which are the primary cells causing damage in Type III reactions. * **Serum Sickness:** Unlike the Arthus reaction, this is a **systemic** Type III reaction (e.g., following antitoxin or penicillin administration).
Question 138: In PCR, why is Thermus aquaticus preferred over E. coli?
- A. Thermostable at the high temperatures required for PCR. (Correct Answer)
- B. Possesses proofreading activity, leading to higher fidelity.
- C. Amplifies DNA more precisely.
- D. Does not require primers for amplification.
Explanation: ### Explanation **1. Why Option A is Correct:** The Polymerase Chain Reaction (PCR) involves a **denaturation step** where the reaction mixture is heated to approximately **94–96°C** to separate double-stranded DNA. DNA polymerase from *E. coli* is mesophilic and would denature (permanently lose function) at these temperatures. In contrast, **Taq polymerase**, derived from the thermophilic bacterium *Thermus aquaticus*, is **thermostable**. It remains active throughout multiple heating cycles, allowing the reaction to proceed without the need to manually add fresh enzyme after every cycle. **2. Why Other Options are Incorrect:** * **Option B:** Standard Taq polymerase actually **lacks 3' to 5' exonuclease activity** (proofreading). This means it has a higher error rate compared to some other polymerases like *Pfu* polymerase. * **Option C:** Precision in PCR is a function of primer specificity and enzyme fidelity. Because Taq lacks proofreading, it is technically *less* precise in terms of sequence accuracy than *E. coli* Polymerase I. * **Option D:** All DNA polymerases, including Taq, require a **free 3'-OH group** provided by a primer to initiate DNA synthesis. **3. High-Yield Clinical Pearls for NEET-PG:** * **Source:** *Thermus aquaticus* is found in hot springs (e.g., Yellowstone National Park). * **Steps of PCR:** Denaturation (95°C) → Annealing (50–65°C) → Extension (72°C). * **Fidelity:** If high fidelity is required (e.g., for cloning), **Pfu polymerase** (from *Pyrococcus furiosus*) is preferred over Taq because it possesses proofreading activity. * **RT-PCR:** Used for RNA viruses (like HIV or SARS-CoV-2); it uses **Reverse Transcriptase** to convert RNA to cDNA before amplification.
Question 139: Which of the following molecular phenomena in Ig genes is responsible for affinity maturation of antibody response?
- A. Chain shuffling
- B. Junctional diversity
- C. Somatic hypermutation (Correct Answer)
- D. Altered RAA splicing
Explanation: **Explanation:** **Somatic Hypermutation (SHM)** is the correct answer. It is the process that occurs in the **germinal centers** of secondary lymphoid organs (lymph nodes and spleen) after an antigen challenge. During B-cell proliferation, point mutations occur at an extremely high rate in the **V (variable) region** genes of heavy and light chains. B-cells with mutations that result in a higher affinity for the antigen are preferentially selected to survive and differentiate into plasma cells. This iterative process is known as **Affinity Maturation**, ensuring that the secondary immune response is more effective than the primary. **Analysis of Incorrect Options:** * **Chain Shuffling:** This refers to the random pairing of different heavy and light chains. While it contributes to initial antibody diversity, it does not drive the refinement of affinity after antigen exposure. * **Junctional Diversity:** This occurs during **V(D)J recombination** in the bone marrow (antigen-independent phase). It involves the random addition or deletion of nucleotides (P and N nucleotides) at the junctions of gene segments. It creates initial diversity but not affinity maturation. * **Altered RNA Splicing:** This mechanism is responsible for the simultaneous expression of **IgM and IgD** on a mature B-cell or the switch from membrane-bound to secreted antibodies. It does not change the idiotype or affinity of the antibody. **High-Yield Clinical Pearls for NEET-PG:** * **Enzyme involved:** **AID (Activation-Induced Cytidine Deaminase)** is essential for both Somatic Hypermutation and Class Switch Recombination. * **Site:** Germinal centers of lymph nodes (specifically the **Dark Zone**). * **Timeline:** Occurs during the **secondary immune response** (IgG/IgA/IgE phase), not the primary IgM phase. * **Distinction:** V(D)J recombination = Antigen-independent (Bone marrow); SHM/Affinity Maturation = Antigen-dependent (Periphery).
Question 140: A 31-year-old male patient complains of fatigue, oral candidiasis, and axillary lymphadenopathy. He reports engaging in high-risk behavior 6 years ago during a trip to eastern and southern Africa. His prior HIV test was reported as negative. Which one of the following diagnostic steps would be most appropriate?
- A. Initiate treatment for HIV disease
- B. Order a test for human T-cell leukemia virus (HTLV)
- C. Repeat the HIV-1 antibody test
- D. Order an HIV test including antibodies to HIV-1 and HIV-2 (Correct Answer)
Explanation: ### Explanation **Correct Answer: D. Order an HIV test including antibodies to HIV-1 and HIV-2** **Rationale:** The patient presents with clinical features suggestive of advanced HIV (oral candidiasis and persistent lymphadenopathy) and a history of high-risk behavior in **Eastern and Southern Africa**. While HIV-1 is the predominant strain globally, **HIV-2** is endemic to parts of Africa (primarily West Africa, but also Southern and Eastern regions). Standard HIV-1 antibody tests do not reliably detect HIV-2 due to significant genetic divergence. A negative prior test for HIV-1 does not rule out HIV-2 infection. Current diagnostic protocols (like the 4th generation ELISA) utilize a combination assay that detects both HIV-1/2 antibodies and the p24 antigen to ensure comprehensive screening. **Analysis of Incorrect Options:** * **A. Initiate treatment:** Antiretroviral therapy (ART) should never be started without a confirmed laboratory diagnosis. Furthermore, HIV-2 is intrinsically resistant to Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs) like Efavirenz, making precise diagnosis crucial for regimen selection. * **B. Test for HTLV:** While HTLV is also a retrovirus found in Africa, it typically presents with Adult T-cell Leukemia/Lymphoma or tropical spastic paraparesis, not opportunistic infections like oral candidiasis. * **C. Repeat HIV-1 antibody test:** If the patient has HIV-2, repeating a specific HIV-1 test will yield another false negative, delaying life-saving treatment. **NEET-PG High-Yield Pearls:** * **HIV-2 Characteristics:** Lower viral load, slower progression, and lower transmissibility compared to HIV-1. * **Drug Resistance:** HIV-2 is **intrinsically resistant to NNRTIs** and has reduced sensitivity to some Protease Inhibitors (PIs). * **Screening Gold Standard:** The 4th generation ELISA (p24 Ag + Ab) reduces the "window period" to approximately 14–21 days. * **Confirmatory Test:** If the screening is positive, a **Multispot HIV-1/HIV-2 rapid antibody differentiation assay** is used to distinguish between the two types.
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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