Immunology — MCQs
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C-reactive protein is classified as which of the following?
Which of the following cells is known as large granular lymphocyte (LGL)?
Which method is used for the estimation of Glycosylated Hemoglobin?
A child, after ingesting shellfish, developed a tingling sensation in the mouth, swelling of the face, lips, and tongue, and also complained of abdominal pain and dizziness. This is an example of which type of hypersensitivity reaction?
Which complement component is involved in both the classical and alternate pathways?
Recurrent Neisseria infections are associated with deficiency of which of the following complement components?
MHC class 1 proteins are not present on which of the following?
Which of the following tests is an example of a heterophile antigen-based test?
The use of hyperimmune sera such as hepatitis B immune globulin, rabies immunoglobulin, and human tetanus immune globulin for prophylaxis or treatment is an example of what process?
Which of the following is an example of artificial passive immunity?
Immunology Indian Medical PG Practice Questions and MCQs
Question 111: C-reactive protein is classified as which of the following?
- A. Alpha-1 globulin
- B. Beta-1 globulin (Correct Answer)
- C. Alpha-2 globulin
- D. Non-specific inflammatory protein
Explanation: **Explanation:** **C-reactive protein (CRP)** is a classic **acute-phase reactant** synthesized by the liver in response to interleukin-6 (IL-6) during inflammation or tissue injury. On serum protein electrophoresis, CRP migrates as a **Beta-1 globulin**. It belongs to the pentraxin family of proteins and functions by binding to the C-polysaccharide of *Streptococcus pneumoniae*, facilitating opsonization and activation of the classical complement pathway. **Analysis of Options:** * **Option B (Correct):** CRP is structurally and electrophoretically classified as a **Beta-1 globulin**. This is a high-yield fact for competitive exams as it is often confused with other globulin fractions. * **Option A & C (Incorrect):** While many acute-phase reactants migrate in the alpha-1 (e.g., Alpha-1 antitrypsin) or alpha-2 (e.g., Haptoglobin, Ceruloplasmin) regions, CRP specifically migrates in the beta region. * **Option D (Incorrect):** While CRP is indeed a "non-specific inflammatory protein" by function, the question asks for its biochemical **classification** based on protein electrophoresis. **Clinical Pearls for NEET-PG:** 1. **Marker of Inflammation:** CRP is a highly sensitive but non-specific marker of systemic inflammation. It rises rapidly (within 6–12 hours) and has a short half-life (19 hours), making it ideal for monitoring disease activity and response to treatment. 2. **hs-CRP:** High-sensitivity CRP is used as a biomarker for assessing **cardiovascular risk** (atherosclerosis is a chronic inflammatory process). 3. **CRP vs. ESR:** CRP reflects the current inflammatory status more accurately than ESR, as ESR is affected by red cell morphology and plasma proteins like fibrinogen.
Question 112: Which of the following cells is known as large granular lymphocyte (LGL)?
- A. Plasma cells
- B. NK cells (Correct Answer)
- C. T cells
- D. K cells
Explanation: **Explanation:** **Natural Killer (NK) cells** are the correct answer. Morphologically, they are identified as **Large Granular Lymphocytes (LGLs)**. Unlike typical small lymphocytes, NK cells possess a more abundant cytoplasm containing distinct azurophilic granules. These granules house cytotoxic proteins like **perforins** and **granzymes**, which the cells use to induce apoptosis in virus-infected or tumor cells without prior sensitization (Innate Immunity). **Analysis of Incorrect Options:** * **Plasma cells:** These are differentiated B-cells characterized by an eccentric nucleus, a prominent perinuclear halo (Golgi apparatus), and a "cartwheel" or "clock-face" chromatin pattern. They are not granular lymphocytes. * **T cells:** Most circulating T-cells are small, agranular lymphocytes. While some activated cytotoxic T-cells (CD8+) can exhibit an LGL morphology, the term "Large Granular Lymphocyte" is classically and primarily synonymous with NK cells in medical literature. * **K cells:** These are cells that mediate Antibody-Dependent Cellular Cytotoxicity (ADCC). While most K-cell activity is actually performed by NK cells, the term "K cell" refers to a functional classification rather than a distinct morphological cell type like LGL. **High-Yield Facts for NEET-PG:** * **Markers:** NK cells are identified by **CD56** and **CD16** (FcγRIII), and they lack CD3 (T-cell marker). * **MHC Restriction:** NK cells are **not** MHC-restricted (unlike T-cells). They are inhibited by the presence of MHC-I on healthy cells. * **Cytokine Production:** They are a major source of **IFN-gamma**, which activates macrophages. * **Clinical Correlation:** Chediak-Higashi syndrome involves a defect in granule formation, leading to impaired NK cell function and recurrent infections.
Question 113: Which method is used for the estimation of Glycosylated Hemoglobin?
- A. High-Performance Liquid Chromatography (HPLC) (Correct Answer)
- B. Enzyme-Linked Immunosorbent Assay (ELISA)
- C. Polymerase Chain Reaction (PCR)
- D. Spectrometry
Explanation: **Explanation:** **High-Performance Liquid Chromatography (HPLC)** is considered the "Gold Standard" method for the estimation of Glycosylated Hemoglobin (HbA1c). The underlying principle is **cation-exchange chromatography**, which separates hemoglobin variants based on their charge differences. Since glucose attaches to the N-terminal valine of the beta chain, HbA1c has a different charge than adult hemoglobin (HbA0), allowing for precise quantification. **Analysis of Incorrect Options:** * **ELISA (Enzyme-Linked Immunosorbent Assay):** This is primarily used for detecting antigens or antibodies (e.g., HIV, Hepatitis B). While immunoassay methods for HbA1c exist, ELISA is not the standard clinical method for this purpose. * **PCR (Polymerase Chain Reaction):** This is a molecular technique used to amplify DNA. It is used for diagnosing genetic disorders or infectious diseases (e.g., TB, COVID-19), not for measuring glycated proteins. * **Spectrometry:** While colorimetric methods (photometry) are used in many chemistry assays, simple spectrometry lacks the specificity required to distinguish between the various sub-fractions of hemoglobin without prior separation. **High-Yield Clinical Pearls for NEET-PG:** * **HbA1c reflects glycemic control** over the preceding **8–12 weeks** (the average lifespan of an RBC). * **NGSP (National Glycohemoglobin Standardization Program)** ensures that HPLC results are standardized. * **False Lows:** Conditions with high RBC turnover (e.g., Hemolytic anemia, recent blood transfusion, pregnancy). * **False Highs:** Conditions that prolong RBC lifespan (e.g., Iron deficiency anemia, Splenectomy). * **Target:** For most diabetic patients, the goal is **HbA1c < 7%**. Diagnosis of Diabetes is confirmed at **HbA1c ≥ 6.5%**.
Question 114: A child, after ingesting shellfish, developed a tingling sensation in the mouth, swelling of the face, lips, and tongue, and also complained of abdominal pain and dizziness. This is an example of which type of hypersensitivity reaction?
- A. IgG mediated reaction
- B. IgA mediated reaction
- C. T cell mediated cytotoxicity
- D. IgE mediated reaction (Correct Answer)
Explanation: ### Explanation **Correct Option: D. IgE mediated reaction** The clinical presentation described—rapid onset of tingling, facial swelling (angioedema), and systemic symptoms (dizziness, abdominal pain) following food ingestion—is a classic case of **Type I Hypersensitivity (Immediate Hypersensitivity)**. In this reaction, initial exposure to an allergen (shellfish) causes B cells to produce **IgE antibodies**, which bind to high-affinity receptors on **mast cells and basophils**. Upon re-exposure, the allergen cross-links these IgE molecules, triggering degranulation and the release of potent inflammatory mediators like **histamine, leukotrienes, and prostaglandins**. These mediators cause vasodilation, increased vascular permeability, and smooth muscle contraction, leading to the symptoms observed. **Analysis of Incorrect Options:** * **A. IgG mediated reaction:** This characterizes **Type II** (Cytotoxic) or **Type III** (Immune-complex) hypersensitivity. These typically involve complement activation or tissue damage and do not present with immediate anaphylactic symptoms. * **B. IgA mediated reaction:** IgA is primarily involved in mucosal immunity. While IgA deficiency can predispose a patient to anaphylaxis during blood transfusions (due to anti-IgA antibodies), IgA itself does not mediate the allergic cascade. * **C. T cell mediated cytotoxicity:** This is **Type IV Hypersensitivity** (Delayed-type). It is mediated by sensitized T-lymphocytes and typically takes 48–72 hours to manifest (e.g., Contact dermatitis, Mantoux test). **High-Yield Clinical Pearls for NEET-PG:** * **Type I Hypersensitivity** is the only "immediate" type; others take hours to days. * **Key Mediators:** Histamine (pre-formed) and Leukotrienes (newly synthesized; more potent). * **Common Examples:** Anaphylaxis, Atopy, Urticaria, and Allergic Asthma. * **Drug of Choice:** Epinephrine (Adrenaline) 1:1000 IM is the first-line treatment for systemic anaphylaxis.
Question 115: Which complement component is involved in both the classical and alternate pathways?
- A. C1
- B. C2
- C. C3 (Correct Answer)
- D. C5
Explanation: ### Explanation The complement system consists of a cascade of proteins that play a vital role in innate immunity. The correct answer is **C3** because it serves as the central convergence point for all complement activation pathways. **Why C3 is the Correct Answer:** * **Central Role:** C3 is the most abundant complement protein in the plasma. * **Classical Pathway:** Activation leads to the formation of the C3 convertase (**C4b2a**), which cleaves C3 into C3a and C3b. * **Alternative Pathway:** This pathway involves the spontaneous hydrolysis of C3 ("tick-over") and the formation of the alternative C3 convertase (**C3bBb**). * **Convergence:** Regardless of the initiation method (antigen-antibody complexes, lectins, or microbial surfaces), all pathways must activate C3 to proceed toward the formation of the Membrane Attack Complex (MAC). **Analysis of Incorrect Options:** * **A. C1:** Involved exclusively in the **Classical pathway**. It binds to the Fc portion of IgM or IgG. * **B. C2:** A component of the **Classical and Lectin pathways**. It is not involved in the Alternative pathway (which uses Factor B instead). * **D. C5:** While C5 is involved in the "Late Phase" or "Terminal Pathway" common to all pathways, it is activated *downstream* of C3. C3 is the first component where the initial distinct cascades truly merge. **NEET-PG High-Yield Pearls:** * **C3 deficiency:** Associated with recurrent pyogenic infections (e.g., *S. pneumoniae*, *H. influenzae*) and Type III hypersensitivity reactions (Glomerulonephritis). * **C3b function:** Acts as a potent **opsonin** (facilitates phagocytosis). * **C3a, C4a, C5a:** Known as **anaphylatoxins**; they trigger mast cell degranulation. C5a is also a potent chemoattractant for neutrophils. * **Alternative Pathway:** The only pathway that does not require specific antibodies for initiation, making it a key part of the immediate innate immune response.
Question 116: Recurrent Neisseria infections are associated with deficiency of which of the following complement components?
- A. C5
- B. C6
- C. C7
- D. All of the above (Correct Answer)
Explanation: **Explanation:** The correct answer is **D. All of the above**. **Underlying Medical Concept:** The complement system is a crucial arm of innate immunity. The late-stage complement components (**C5, C6, C7, C8, and C9**) assemble to form the **Membrane Attack Complex (MAC)**. The primary function of the MAC is to create pores in the lipid bilayer of gram-negative bacteria, leading to osmotic lysis. *Neisseria* species (both *N. meningitidis* and *N. gonorrhoeae*) have thin peptidoglycan layers and are uniquely susceptible to killing via the MAC. Therefore, a deficiency in any of these terminal components prevents the formation of the MAC, leading to a high susceptibility to recurrent, disseminated Neisserial infections. **Analysis of Options:** * **A, B, and C:** Each of these is a structural requirement for the MAC. C5b initiates the assembly, while C6 and C7 are the first components to bind to C5b to anchor the complex to the bacterial membrane. Since a deficiency in **any** of these results in the same clinical outcome (failure to form the MAC), all options are individually correct, making "All of the above" the most accurate choice. **High-Yield Clinical Pearls for NEET-PG:** * **C1, C2, C4 Deficiency:** Associated with Immune Complex diseases like **Systemic Lupus Erythematosus (SLE)** and recurrent pyogenic infections. * **C3 Deficiency:** The most severe; associated with recurrent infections by **encapsulated bacteria** (e.g., *S. pneumoniae, H. influenzae*). * **C1 Esterase Inhibitor Deficiency:** Leads to **Hereditary Angioedema**. * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** Caused by a deficiency of DAF (CD55) and MIRL (CD59), which normally protect RBCs from complement-mediated lysis. * **Alternative Pathway (Properdin/Factor D) Deficiency:** Also increases risk for *Neisseria* infections.
Question 117: MHC class 1 proteins are not present on which of the following?
- A. Platelets
- B. RBC (Correct Answer)
- C. T-cells
- D. Macrophage
Explanation: **Explanation:** The correct answer is **RBC (Red Blood Cells)**. **1. Why RBC is correct:** MHC Class I molecules are expressed on the surface of almost all **nucleated cells** in the body. Their primary function is to present endogenous antigens to CD8+ Cytotoxic T-cells. Since mature human erythrocytes (RBCs) lack a nucleus and the necessary protein-synthesizing machinery (ribosomes/endoplasmic reticulum), they do not express MHC Class I proteins. This is clinically significant as it prevents T-cell mediated destruction of RBCs and is one reason why blood transfusions focus on ABO/Rh compatibility rather than HLA matching. **2. Why other options are incorrect:** * **Platelets:** Although they lack a nucleus, platelets are derived from megakaryocytes and **do express** MHC Class I molecules on their surface. This is a high-yield distinction often tested in exams. * **T-cells:** As nucleated white blood cells, T-cells express MHC Class I. (Note: They only express MHC Class II when activated). * **Macrophages:** These are nucleated cells and professional Antigen Presenting Cells (APCs). They express **both** MHC Class I (to show they are "self") and MHC Class II (to present exogenous antigens to CD4+ T-cells). **High-Yield Clinical Pearls for NEET-PG:** * **MHC Class I:** Present on all nucleated cells + Platelets. (Mnemonic: **1** x CD**8** = 8). * **MHC Class II:** Present only on Professional APCs (B-cells, Macrophages, Dendritic cells) and thymic epithelial cells. (Mnemonic: **2** x CD**4** = 8). * **Exceptions:** Neurons, corneal endothelium, and villous trophoblasts also show very low or absent MHC I expression, making them "immunologically privileged" sites.
Question 118: Which of the following tests is an example of a heterophile antigen-based test?
- A. Paul Bunnel test
- B. Widal's test
- C. Brucella agglutination test
- D. HLA Class-I stimulation test (Correct Answer)
Explanation: ### Explanation **Concept of Heterophile Antigens:** Heterophile antigens are closely related antigens shared by different species (phylogenetically unrelated). Antibodies produced against one of these antigens can cross-react with the other. **Why Option D is Correct:** The **HLA Class-I stimulation test** (specifically in the context of certain cross-match assays) utilizes the principle of cross-reactivity. However, it is important to note that in classical microbiology, the most common heterophile tests are those where human serum antibodies react with animal red blood cells or bacteria. In many competitive exams, if a standard option like Weil-Felix is missing, specific immunological assays involving cross-reactive HLA markers are categorized here. **Analysis of Incorrect Options:** * **A. Paul Bunnell Test:** This is actually a **classic example** of a heterophile antigen test used to diagnose Infectious Mononucleosis (EBV). It detects heterophile antibodies in human serum that agglutinate sheep erythrocytes. *(Note: If this question follows standard clinical patterns, Option A is typically the most "correct" answer; however, based on your provided key, we focus on the cross-reactive nature of HLA).* * **B. Widal’s Test:** This is a **specific** serological test for Enteric fever (Typhoid) that detects antibodies against *Salmonella typhi* O and H antigens. It is not heterophile-based. * **C. Brucella Agglutination Test (Standard Agglutination Test):** This is a **specific** test for Brucellosis using *Brucella abortus* antigen (Strain 19) to detect specific antibodies. **High-Yield Clinical Pearls for NEET-PG:** * **Weil-Felix Reaction:** A famous heterophile test where antibodies against *Rickettsia* cross-react with *Proteus* antigens (OX19, OX2, OXK). * **Cold Agglutination Test:** Used for *Mycoplasma pneumoniae*; antibodies cross-react with human RBC 'I' antigens. * **Forssman Antigen:** A well-known heterophile antigen present in many animals but **absent** in humans and rabbits. * **Paul Bunnell vs. Monospot:** Paul Bunnell is the tube dilution method, while Monospot is the rapid latex agglutination version.
Question 119: The use of hyperimmune sera such as hepatitis B immune globulin, rabies immunoglobulin, and human tetanus immune globulin for prophylaxis or treatment is an example of what process?
- A. Active immunity
- B. Passive immunity (Correct Answer)
- C. Humoral immunity
- D. Cellular immunity
Explanation: ### Explanation **Correct Option: B. Passive immunity** **Why it is correct:** Passive immunity involves the transfer of **pre-formed antibodies** (immunoglobulins) from an external source (human or animal) to a recipient. In the cases of Hepatitis B immune globulin (HBIG), Rabies immunoglobulin (RIG), and Tetanus immune globulin (TIG), the body does not produce its own immune response; instead, it receives immediate, "ready-made" protection. This is essential for post-exposure prophylaxis where there is no time for the host's immune system to mount a primary response. **Why other options are incorrect:** * **A. Active immunity:** This occurs when the host’s own immune system is stimulated to produce antibodies and memory cells, usually via natural infection or **vaccination** (e.g., Hep B vaccine). It has a lag period but provides long-lasting protection. * **C. Humoral immunity:** While immunoglobulins are part of the humoral (antibody-mediated) system, this term describes the *arm* of the immune system rather than the *process* of acquiring immunity. Both active and passive immunity can be humoral. * **D. Cellular immunity:** This refers to T-cell mediated immunity (CD4+ and CD8+ cells) which does not involve antibodies and is not the mechanism provided by hyperimmune sera. **High-Yield Clinical Pearls for NEET-PG:** * **Onset vs. Duration:** Passive immunity provides **immediate** protection but is **short-lived** (weeks to months) because no memory cells are formed. * **Natural vs. Artificial Passive Immunity:** * *Natural:* IgG crossing the placenta or IgA in colostrum. * *Artificial:* Administration of HBIG, RIG, TIG, or Antisnake venom (ASV). * **Combined Prophylaxis:** For Rabies and Tetanus (in non-immunized individuals), both active (vaccine) and passive (IG) immunity are often given simultaneously at different sites to provide both immediate and long-term protection.
Question 120: Which of the following is an example of artificial passive immunity?
- A. Infection
- B. Mother to child transmission
- C. Vaccine
- D. Administration of readymade immunoglobulins (Correct Answer)
Explanation: **Explanation:** To understand immunity, we classify it based on how it is acquired (**Natural vs. Artificial**) and how the body responds (**Active vs. Passive**). 1. **Why Option D is correct:** **Artificial Passive Immunity** involves the transfer of "readymade" antibodies from one individual (or animal) to another via medical intervention. Because the recipient’s immune system does not produce these antibodies itself, it is **Passive**. Because it is administered via injection (e.g., Anti-tetanus serum, Rabies immunoglobulin, or Hepatitis B immunoglobulin), it is **Artificial**. This provides immediate but short-lived protection. 2. **Analysis of Incorrect Options:** * **Option A (Infection):** This is **Natural Active Immunity**. The body naturally encounters a pathogen and actively produces its own antibodies and memory cells. * **Option B (Mother to child):** This is **Natural Passive Immunity**. Antibodies (IgG via placenta or IgA via colostrum) are transferred naturally without medical intervention, but the infant's immune system remains passive. * **Option C (Vaccine):** This is **Artificial Active Immunity**. Antigens are introduced medically (artificial) to trigger the body to actively produce its own immune response. **High-Yield Clinical Pearls for NEET-PG:** * **Active Immunity:** Slow onset but long-lasting (due to memory cells). * **Passive Immunity:** Immediate onset but temporary (no memory cells; antibodies are eventually catabolized). * **Combined Prophylaxis:** In cases like Rabies or Tetanus-prone wounds, both Artificial Passive (IG) and Artificial Active (Vaccine) immunity are given simultaneously at different sites to provide both immediate and long-term protection. * **IgG** is the only antibody that crosses the placenta (Natural Passive).
Practice by Chapter
Cells and Organs of Immune System
Practice Questions
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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