Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 341: Which one of the following statements regarding hypersensitivity reactions is FALSE?

A. Theobald-Smith phenomenon is a Type I hypersensitivity reaction.
B. Serum sickness is a Type II hypersensitivity reaction. (Correct Answer)
C. Allograft rejection is a Type IV hypersensitivity reaction.
D. Transfusion reaction is a Type II hypersensitivity reaction.

Explanation: **Explanation:** The correct answer is **B** because **Serum sickness is a Type III hypersensitivity reaction**, not Type II. **Understanding the Concept:** Hypersensitivity reactions are classified by the Gell and Coombs system. **Type III (Immune Complex-mediated)** reactions occur when soluble antigen-antibody complexes deposit in tissues (like blood vessels or joints), activating the complement system and causing systemic inflammation. Serum sickness typically occurs after the administration of foreign proteins (e.g., anti-thymocyte globulin or snake antivenom), leading to fever, rash, and arthralgia. **Analysis of Other Options:** * **Option A (True):** The **Theobald-Smith phenomenon** refers to experimental systemic anaphylaxis in guinea pigs, which is a classic example of a **Type I (IgE-mediated)** reaction. * **Option C (True):** **Allograft rejection** (specifically acute and chronic cellular rejection) is primarily mediated by T-cells, making it a **Type IV (Delayed-type)** hypersensitivity reaction. * **Option D (True):** **Transfusion reactions** (ABO incompatibility) involve antibodies (IgM/IgG) binding to antigens on the surface of red blood cells, leading to complement-mediated lysis. This is a hallmark of **Type II (Cytotoxic)** hypersensitivity. **High-Yield Clinical Pearls for NEET-PG:** * **Type II vs. Type III:** Remember, Type II involves antigens fixed **on cell surfaces** (e.g., Myasthenia Gravis, Goodpasture syndrome), while Type III involves **soluble** antigens forming circulating complexes (e.g., SLE, Post-streptococcal glomerulonephritis). * **Arthus Reaction:** This is the localized form of Type III hypersensitivity, whereas Serum Sickness is the systemic form. * **Mnemonic for Gell & Coombs:** **ACID** (Type I: **A**nanphylactic/Atopic; Type II: **C**ytotoxic; Type III: **I**mmune Complex; Type IV: **D**elayed).

Question 342: Which IgG subclass exhibits the greatest individual variation?

A. IgG1 (Correct Answer)
B. IgG2
C. IgG3
D. IgG4

Explanation: **Explanation:** The correct answer is **IgG1**. In human serum, IgG is the most abundant immunoglobulin class, further divided into four subclasses based on structural differences in their heavy chain constant regions. **Why IgG1 is correct:** IgG1 is the most predominant subclass, accounting for approximately **60-70%** of total serum IgG. Because it is the most abundant, it exhibits the **greatest individual variation** in absolute serum concentration among different people. While all IgG subclasses have genetic variants (allotypes), the sheer volume and primary role of IgG1 in the immune response to protein antigens make its quantitative fluctuations most prominent in clinical profiles. **Analysis of Incorrect Options:** * **IgG2:** This is the second most common subclass (approx. 20%). It is primarily involved in the immune response against polysaccharide antigens (e.g., *S. pneumoniae*). Deficiencies in IgG2 are common in children with recurrent sinopulmonary infections. * **IgG3:** Known for having the longest hinge region and being the most effective complement activator. However, it has a much shorter half-life (7 days) compared to the others (23 days) and lower serum concentration. * **IgG4:** The least abundant subclass (<5%). It is unique because it can undergo "half-molecule exchange," making it functionally monovalent. It does not activate complement and is often associated with chronic allergen exposure or IgG4-related diseases. **High-Yield NEET-PG Pearls:** * **Abundance Order:** IgG1 > IgG2 > IgG3 > IgG4. * **Placental Transfer:** IgG1 is transferred most efficiently across the placenta (IgG2 is the least efficient). * **Complement Activation:** IgG3 is the most potent activator, followed by IgG1 and IgG2 (IgG4 does not activate complement). * **Half-life:** All IgG subclasses have a half-life of ~23 days, **except IgG3**, which lasts only ~7 days.

Question 343: Which of the following class-specific antigenic determinants of an immunoglobulin is associated with the H-chain?

A. L-chain
B. H-chain (Correct Answer)
C. J-chain
D. Variable region

Explanation: ### Explanation The classification of immunoglobulins into five distinct classes (IgG, IgA, IgM, IgD, and IgE) is determined by the **Isotypic determinants**. These determinants are based on the constant region of the **Heavy (H) chain**. **Why the H-chain is correct:** Immunoglobulins are defined by their heavy chain type: $\gamma$ (gamma) for IgG, $\alpha$ (alpha) for IgA, $\mu$ (mu) for IgM, $\delta$ (delta) for IgD, and $\epsilon$ (epsilon) for IgE. Because these antigenic differences are located in the constant region of the heavy chain, the H-chain is the structural component that dictates the class-specific identity and biological effector functions (like complement fixation or placental transfer). **Analysis of Incorrect Options:** * **L-chain (Light chain):** There are only two types of light chains ($\kappa$ and $\lambda$). Both types can be found in any class of immunoglobulin; therefore, they do not determine the specific class. * **J-chain (Joining chain):** This is a polypeptide found only in polymeric forms of antibodies (secretory IgA and pentameric IgM). It facilitates polymerization but does not define the immunoglobulin class itself. * **Variable region:** This region (found on both H and L chains) is responsible for antigen-binding specificity (idiotypes), not for determining the class (isotype) of the antibody. **High-Yield NEET-PG Pearls:** * **Isotypes:** Determined by Heavy chain constant regions (defines Class). * **Allotypes:** Determined by allelic differences at specific loci (individual variations within a species). * **Idiotypes:** Determined by the hypervariable regions in the Fab portion (unique to a specific antigen-binding site). * **Memory Trick:** **H**eavy chain = **H**ierarchy (Class/Isotype).

Question 344: What is the most common site of angioedema?

A. Hands
B. Lips (Correct Answer)
C. Eyelid
D. Abdomen

Explanation: **Explanation:** Angioedema is characterized by a self-limiting, localized, and deep swelling of the submucosal or subcutaneous tissues. This occurs due to increased vascular permeability, often mediated by histamine (Type I Hypersensitivity) or bradykinin (e.g., ACE inhibitor-induced or Hereditary Angioedema). **Why Lips are the Correct Answer:** The **lips** are the most frequently involved site in angioedema. This is because the facial area has a high density of mast cells and loose connective tissue, which allows for rapid fluid accumulation. In clinical practice and emergency presentations, the "classic" appearance of angioedema involves the lips and the periorbital region. **Analysis of Incorrect Options:** * **Hands (Option A):** While the dorsum of the hands and feet are common sites for peripheral swelling, they are less frequently involved than the face in acute allergic angioedema. * **Eyelid (Option C):** The eyelids (periorbital area) are the second most common site. While frequently involved alongside the lips, the lips remain the statistically dominant site of presentation. * **Abdomen (Option D):** Abdominal involvement (bowel wall edema) is a hallmark of **Hereditary Angioedema (HAE)** due to C1 esterase inhibitor deficiency. While high-yield for exams, it is not the "most common" site overall compared to facial involvement. **NEET-PG High-Yield Pearls:** 1. **Hereditary Angioedema (HAE):** Characterized by low C4 levels (best screening test) and deficiency of C1 esterase inhibitor. It typically does **not** present with urticaria (hives). 2. **Drug-Induced:** ACE inhibitors (e.g., Enalapril) are a common cause of bradykinin-mediated angioedema. 3. **Life-threatening Complication:** Laryngeal edema is the most feared complication, leading to airway obstruction.

Question 345: Termination of protein synthesis is performed by all except:

A. Releasing factor
B. Stop codon
C. Peptidyl transferase (Correct Answer)
D. UAA codon

Explanation: ### Explanation The process of translation (protein synthesis) occurs in three stages: initiation, elongation, and termination. **Why Peptidyl Transferase is the Correct Answer:** Peptidyl transferase is an enzyme (specifically a ribozyme located in the large ribosomal subunit) responsible for **elongation**, not termination. Its primary role is to catalyze the formation of peptide bonds between adjacent amino acids by transferring the growing polypeptide chain from the P-site tRNA to the amino acid on the A-site tRNA. Since it functions during the growth phase of the protein chain, it does not terminate the process. **Analysis of Incorrect Options:** * **Stop Codons (B and D):** Termination begins when a nonsense or "stop" codon enters the A-site of the ribosome. There are three stop codons: **UAA** (Ochre), **UAG** (Amber), and **UGA** (Opal). These do not code for any amino acid. * **Releasing Factors (A):** Since there are no tRNA molecules that recognize stop codons, proteins called **Releasing Factors (RF1, RF2, and RF3)** recognize these signals. They bind to the ribosome and trigger the hydrolysis of the bond between the completed polypeptide and the tRNA, effectively terminating synthesis. **High-Yield Clinical Pearls for NEET-PG:** * **Ribozyme Activity:** In prokaryotes, the peptidyl transferase activity is associated with the **23S rRNA** of the 50S subunit. * **Antibiotic Correlation:** **Chloramphenicol** acts by inhibiting the peptidyl transferase enzyme, thereby preventing protein elongation in bacteria. * **Energy Requirement:** Termination is an energy-dependent process requiring the hydrolysis of **GTP**. * **Mnemonic for Stop Codons:** * **UAA**: **U** Are **A**way * **UAG**: **U** Are **G**one * **UGA**: **U** Go **A**way

Question 346: Chronic granulomatous disorder is due to a defect in which component?

A. B-cells
B. NADPH oxidase (Correct Answer)
C. IgA
D. T-cell

Explanation: **Explanation:** **Chronic Granulomatous Disease (CGD)** is a primary immunodeficiency caused by a genetic defect in the **NADPH oxidase enzyme complex** within phagocytes (neutrophils and macrophages). 1. **Mechanism (Why B is correct):** Under normal conditions, NADPH oxidase facilitates the "respiratory burst" by converting molecular oxygen into superoxide radicals. These radicals are essential for producing reactive oxygen species (ROS) like hydrogen peroxide and hypochlorite, which kill ingested pathogens. In CGD, this oxidative killing mechanism is absent. Consequently, phagocytes can ingest bacteria but cannot kill them, leading to the formation of **granulomas** as the body attempts to wall off the persistent infection. 2. **Why other options are incorrect:** * **A & C (B-cells and IgA):** These relate to humoral immunity. Defects here lead to conditions like Agammaglobulinemia or Selective IgA deficiency, characterized by sinopulmonary infections, not granulomatous inflammation. * **D (T-cells):** T-cell defects (e.g., DiGeorge Syndrome) primarily result in increased susceptibility to viral, fungal, and protozoal infections due to impaired cell-mediated immunity. **High-Yield Clinical Pearls for NEET-PG:** * **Pathogens:** Patients are highly susceptible to **Catalase-positive organisms** (e.g., *Staphylococcus aureus, Aspergillus, Nocardia, Serratia marcescens, Burkholderia cepacia*). Catalase-negative organisms are killed normally because the phagocyte "borrows" the H₂O₂ produced by the bacteria itself. * **Diagnosis:** The gold standard is the **Dihydrorhodamine (DHR) flow cytometry test** (shows decreased fluorescence). The classic **Nitroblue Tetrazolium (NBT) dye test** remains negative (fails to turn blue). * **Inheritance:** Most commonly **X-linked recessive** (defect in the *gp91phox* subunit).

Question 347: Synthesis of membrane-bound or secretory forms of an immunoglobulin is determined by?

A. One turn to two turn joining rule
B. Class switching
C. Differential RNA processing (Correct Answer)
D. Allelic exclusion

Explanation: ### Explanation The correct answer is **Differential RNA processing** (also known as alternative splicing). #### 1. Why Differential RNA Processing is Correct A single B-cell can produce an immunoglobulin (Ig) in two forms: **membrane-bound** (acting as a B-cell receptor) or **secreted** (as an antibody). This choice is determined at the **RNA level**, not the DNA level. The heavy chain gene contains two distinct polyadenylation (poly-A) sites at its 3' end. * If the first site is used, the mRNA excludes the hydrophobic transmembrane segment, resulting in a **secretory Ig**. * If the second site is used, the mRNA includes the transmembrane segment, resulting in a **membrane-bound Ig**. Since this occurs via alternative splicing of the primary RNA transcript, it is a post-transcriptional process. #### 2. Why Other Options are Incorrect * **A. One turn to two turn joining rule (12/23 rule):** This ensures that V, D, and J gene segments join in the correct order during somatic recombination. It does not determine the physical form (secretory vs. membrane) of the Ig. * **B. Class switching (Isotype switching):** This involves DNA recombination to change the constant region (e.g., from IgM to IgG). It changes the *class* of the antibody but not whether it is membrane-bound or secreted. * **C. Allelic exclusion:** This process ensures that a B-cell expresses an immunoglobulin from only one of its two parental alleles, ensuring monoclonal specificity. #### 3. High-Yield Clinical Pearls for NEET-PG * **DNA Level Changes:** VDJ recombination and Class Switching (Irreversible). * **RNA Level Changes:** Synthesis of membrane vs. secretory forms and the simultaneous expression of IgM and IgD on mature B-cells (Reversible/Differential processing). * **Key Enzyme:** **AID** (Activation-induced cytidine deaminase) is essential for Class Switching and Somatic Hypermutation, but *not* for differential RNA processing.

Question 348: Which portion of the MHC class I complex forms the antigen-presenting part?

A. Between alpha 1 and beta 2 microglobulin
B. Distal part of the alpha chain (Correct Answer)
C. Proximal part of the alpha chain
D. Between alpha subunit and beta 2 microglobulin

Explanation: **Explanation:** The **MHC Class I molecule** is a heterodimer consisting of a heavy **$\alpha$ (alpha) chain** (with three domains: $\alpha$1, $\alpha$2, and $\alpha$3) and a light chain called **$\beta$2-microglobulin**. The **antigen-binding cleft** (the site where endogenous peptides are presented to CD8+ T-cells) is formed by the folding of the **$\alpha$1 and $\alpha$2 domains**. These two domains are located at the **distal (outermost) end** of the molecule, furthest from the cell membrane. Therefore, the distal part of the alpha chain forms the antigen-presenting part. **Analysis of Options:** * **Option A & D:** $\beta$2-microglobulin does not participate in forming the peptide-binding groove. Its primary role is to provide structural support and stabilize the MHC-I complex on the cell surface. * **Option C:** The proximal part of the alpha chain refers to the **$\alpha$3 domain**, which is located closest to the cell membrane. This domain is highly conserved and serves as the binding site for the **CD8 co-receptor** of T-cells, rather than the antigen itself. **High-Yield Facts for NEET-PG:** * **MHC Class I:** Presents **endogenous antigens** (e.g., viral or tumor proteins) to **CD8+ Cytotoxic T-cells**. Found on all nucleated cells. * **MHC Class II:** Antigen-binding cleft is formed by **$\alpha$1 and $\beta$1 domains**. It presents **exogenous antigens** to **CD4+ Helper T-cells**. Found only on Professional Antigen Presenting Cells (APCs). * **Rule of 8:** MHC I × CD8 = 8; MHC II × CD4 = 8. * **Human Leukocyte Antigens (HLA):** MHC Class I corresponds to HLA-A, B, and C.

Question 349: HIV primarily affects which of the following cells?

A. CD4 cells (Correct Answer)
B. CD8 cells
C. Natural killer cells
D. Helper cells

Explanation: **Explanation:** The Human Immunodeficiency Virus (HIV) is a retrovirus that specifically targets cells expressing the **CD4 molecule** on their surface. The viral envelope glycoprotein **gp120** binds with high affinity to the CD4 receptor, using co-receptors like **CCR5** (macrophages/early infection) or **CXCR4** (T-cells/late infection) to enter the cell. While "Helper T-cells" are the most famous CD4+ cells, the term **CD4 cells** is the most accurate answer because HIV also infects other CD4-expressing cells such as macrophages, monocytes, and dendritic cells. **Analysis of Options:** * **CD4 cells (Correct):** This is the primary target. The progressive depletion of these cells leads to profound immunodeficiency and AIDS. * **CD8 cells:** These are cytotoxic T-cells. They do not possess the CD4 receptor required for gp120 binding; in fact, CD8 cells initially increase in number to fight the HIV infection before eventually declining due to a lack of "help" from CD4 cells. * **Natural Killer (NK) cells:** These are part of the innate immune system. While their function is impaired in chronic HIV infection, they are not the primary target for viral entry. * **Helper cells:** While HIV does infect T-helper cells, "CD4 cells" is a more comprehensive term in microbiology as it encompasses non-T-cell targets (macrophages/monocytes) which act as viral reservoirs. **Clinical Pearls for NEET-PG:** * **Marker of Progression:** The absolute CD4+ T-cell count is the best indicator of the stage of HIV progression and the risk for opportunistic infections (e.g., *Pneumocystis jirovecii* when CD4 <200). * **Viral Entry:** gp120 is for **attachment**; gp41 is for **fusion** and entry. * **Reservoirs:** Macrophages and Microglial cells (in the CNS) serve as important long-term reservoirs for HIV.

Question 350: Antibody-dependent cell-mediated cytotoxicity (ADCC) is seen with which of the following cells?

A. T cells
B. B cells
C. NK cells (Correct Answer)
D. Neutrophils

Explanation: ### Explanation **Antibody-dependent cell-mediated cytotoxicity (ADCC)** is a mechanism of cell-mediated immune defense whereby an effector cell of the immune system actively lyses a target cell, whose membrane-surface antigens have been bound by specific antibodies (usually IgG). **Why NK cells are the correct answer:** Natural Killer (NK) cells are the primary mediators of ADCC. They express a specific surface receptor called **CD16 (FcγRIII)**. This receptor recognizes and binds to the Fc portion of IgG antibodies that are already attached to a target cell (such as a virus-infected or tumor cell). Once bound, the NK cell releases cytotoxins like **perforins and granzymes**, leading to apoptosis of the target cell. **Analysis of Incorrect Options:** * **T cells:** Cytotoxic T cells (CD8+) kill targets via MHC-I recognition, not via antibody-binding (ADCC). While a small subset of T cells may show minor activity, they are not the classic mediators of this process. * **B cells:** These are part of the humoral immune system responsible for *producing* antibodies, not for cell-mediated killing via ADCC. * **Neutrophils:** While neutrophils and eosinophils possess Fc receptors and can technically participate in ADCC (especially against helminths), **NK cells** are the most potent and "classic" example tested in medical examinations. **High-Yield Clinical Pearls for NEET-PG:** * **Effector Cells in ADCC:** NK cells (most common), Macrophages, Monocytes, Neutrophils, and Eosinophils (specifically against parasites via IgE). * **Key Receptor:** **CD16** is the marker for ADCC. * **Antibody involved:** Primarily **IgG** (IgE in the case of eosinophils). * **Mechanism:** Unlike direct NK cell killing, ADCC is **antigen-specific** because it relies on the specificity of the antibody bound to the target.

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Immunology — MCQs

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