Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 81: Which complement complex attacks the cell membrane?

A. C12345
B. C23456
C. C34567
D. C56789 (Correct Answer)

Explanation: ### Explanation **Correct Option: D (C56789)** The correct answer is **C56789**, which represents the **Membrane Attack Complex (MAC)**. This is the final common pathway for all three complement activation routes (Classical, Alternative, and Lectin). * **Mechanism:** The process begins when C5 convertase cleaves C5 into C5a and C5b. **C5b** then binds sequentially with **C6, C7, and C8**. Finally, multiple **C9** molecules polymerize to form a hollow transmembrane channel (pore). * **Result:** This pore disrupts the osmotic integrity of the target cell, leading to an influx of water and ions, resulting in **osmotic lysis** and cell death. **Why Other Options are Incorrect:** * **Options A, B, and C:** These represent arbitrary sequences of complement proteins. While C1, C2, C3, and C4 are essential upstream components (opsonization and anaphylatoxin production), they do not directly insert into the lipid bilayer to form a lytic pore. Specifically, C3 is the most abundant complement but acts as a "central hub" rather than the terminal effector. **High-Yield Clinical Pearls for NEET-PG:** * **Neisserial Infections:** Patients with deficiencies in the terminal complement components (**C5-C9**) are uniquely susceptible to recurrent systemic infections by *Neisseria meningitidis* and *Neisseria gonorrhoeae*. * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** Caused by a deficiency of DAF (CD55) and MIRL (CD59). CD59 normally inhibits the assembly of the MAC; its absence leads to complement-mediated RBC lysis. * **C3 Deficiency:** This is the most severe complement deficiency, as it predisposes to infections with encapsulated bacteria (e.g., *S. pneumoniae*) and Type III hypersensitivity reactions.

Question 82: Heterophile antibody is found in which test?

A. Weil Felix test (Correct Answer)
B. Widal test
C. VDRL
D. None of the above

Explanation: **Explanation:** The **Weil-Felix test** is a classic example of a **heterophile antibody test**. Heterophile antibodies are antibodies produced against one antigen that cross-react with a completely different antigen found in another species. In this case, antibodies produced during certain **Rickettsial infections** cross-react with the somatic (O) antigens of specific strains of **Proteus vulgaris** (OX-19, OX-2) and **Proteus mirabilis** (OX-K). This agglutination reaction helps in the presumptive diagnosis of typhus and spotted fever groups. **Analysis of Options:** * **Weil-Felix Test (Correct):** Uses Proteus antigens to detect Rickettsial antibodies. It is a heterophile agglutination test. * **Widal Test:** This is a specific serological test used to detect antibodies against *Salmonella typhi* and *paratyphi* (Enteric fever). It uses specific H and O antigens of the Salmonella bacteria itself, not heterophile antigens. * **VDRL (Venereal Disease Research Laboratory):** This is a non-specific screening test for Syphilis. While it uses **Cardiolipin** (an extract from beef heart) to detect Reagin antibodies, it is classified as a non-treponemal flocculation test rather than a classic heterophile agglutination test like Weil-Felix. **High-Yield Clinical Pearls for NEET-PG:** * **Paul-Bunnell Test:** Another high-yield heterophile antibody test used for diagnosing **Infectious Mononucleosis** (EBV), where patient serum agglutinates sheep RBCs. * **Weil-Felix Patterns:** * **Epidemic/Endemic Typhus:** OX-19 positive. * **Scrub Typhus:** OX-K positive. * **Rocky Mountain Spotted Fever:** OX-19 and OX-2 positive. * **Q Fever:** Negative for Weil-Felix (No heterophile antibodies produced).

Question 83: Which of the following statements is true regarding the Major Basic Protein?

A. Formed by eosinophils.
B. Cytotoxic to parasites.
C. Not very effective against bacteria.
D. All the above. (Correct Answer)

Explanation: **Explanation:** **Major Basic Protein (MBP)** is a highly specialized, potent cytotoxic protein stored within the large crystalline granules of **eosinophils**. It plays a pivotal role in the innate immune response, particularly against multicellular pathogens. 1. **Formed by Eosinophils (Option A):** MBP is the most abundant protein found in the core of eosinophil granules. It is synthesized as a pro-protein and stored in its active form, ready for rapid release during degranulation. 2. **Cytotoxic to Parasites (Option B):** MBP is the primary weapon against helminths (parasitic worms). It acts by binding to the negatively charged surface of the parasite, causing membrane disruption and tegumental damage. This is the hallmark of the eosinophil-mediated defense mechanism. 3. **Not very effective against Bacteria (Option C):** While MBP has some non-specific toxic effects, its primary evolutionary design is for large, non-phagocytosable targets like helminths. It lacks the specific bactericidal efficiency seen in neutrophil-derived proteins like myeloperoxidase or defensins. **Clinical Pearls for NEET-PG:** * **Eosinophilia:** Characteristically seen in **NAACP** (Neoplasia, Asthma, Allergy, Collagen vascular diseases, and Parasites). * **Charcot-Leyden Crystals:** These are formed from the breakdown of eosinophils (specifically Galectin-10) and are found in the sputum of asthmatics. * **Other Eosinophil Granules:** Besides MBP, eosinophils contain Eosinophil Cationic Protein (ECP), Eosinophil Peroxidase (EPO), and Eosinophil-Derived Neurotoxin (EDN). * **MBP and Tissue Damage:** While protective against parasites, the release of MBP in the airways is a major cause of epithelial damage in **Bronchial Asthma**.

Question 84: Which of the following is the most important antigen-presenting cell (APC) for initiating T-cell response against protein antigens?

A. NK cell
B. Dendritic cell (Correct Answer)
C. Macrophage
D. B-lymphocyte

Explanation: **Explanation:** The correct answer is **B. Dendritic cell**. **Why Dendritic Cells are the most important APCs:** Dendritic cells (DCs) are considered the "professional" and most potent antigen-presenting cells for initiating **primary T-cell responses**. Their superiority lies in their unique ability to capture antigens in peripheral tissues, migrate to regional lymph nodes, and express high levels of **MHC Class II** and **co-stimulatory molecules** (like B7-1 and B7-2). Unlike other APCs, mature dendritic cells are the only cells capable of activating **naive T-lymphocytes**, thereby bridging innate and adaptive immunity. **Analysis of Incorrect Options:** * **A. NK cell:** Natural Killer cells are part of the innate immune system involved in killing virally infected or tumor cells. They are **not** antigen-presenting cells. * **C. Macrophage:** While macrophages are professional APCs, their primary role is to present antigens to **already differentiated effector T-cells** to enhance their own microbicidal activity (cell-mediated immunity), rather than initiating a primary response. * **D. B-lymphocyte:** B-cells act as APCs by presenting antigens to **Helper T-cells (CD4+)** to receive signals for antibody production (humoral immunity). They are not the primary initiators of the systemic T-cell response. **High-Yield NEET-PG Pearls:** * **Langerhans cells** are specialized dendritic cells found in the epidermis. * **Follicular Dendritic Cells (FDCs)** are found in germinal centers; they trap antigens for B-cells but, interestingly, do **not** express MHC Class II. * The most potent stimulator of naive T-cells is the **Mature Dendritic Cell**. * **Cross-presentation:** A unique feature of certain DCs where they present exogenous antigens via MHC Class I to CD8+ T-cells.

Question 85: Allergic hypersensitivity is mediated by which immunoglobulin?

A. IgM
B. IgG
C. IgD
D. IgE (Correct Answer)

Explanation: **Explanation:** **IgE (Immunoglobulin E)** is the primary mediator of Type I (Immediate) hypersensitivity reactions. When an individual is exposed to an allergen, IgE antibodies are produced and bind to high-affinity receptors (FcεRI) on the surface of **mast cells and basophils**. Upon re-exposure, the allergen cross-links these bound IgE molecules, triggering degranulation and the release of inflammatory mediators like histamine, leukotrienes, and prostaglandins. This leads to clinical manifestations such as anaphylaxis, asthma, and hay fever. **Why other options are incorrect:** * **IgM:** This is the first antibody produced in a primary immune response. It is involved in Type II and Type III hypersensitivity but is not the mediator of allergic/atopic reactions. * **IgG:** The most abundant circulating antibody, it provides long-term immunity and crosses the placenta. While it can mediate Type II (cytotoxic) and Type III (immune-complex) hypersensitivity, it does not trigger the classic allergic cascade. * **IgD:** Found primarily on the surface of B-cells, its exact function is less defined but it acts mainly as an antigen receptor for B-cell activation; it has no role in hypersensitivity. **High-Yield Clinical Pearls for NEET-PG:** * **Prausnitz-Küstner (PK) Reaction:** A classic test used to demonstrate IgE-mediated hypersensitivity via serum transfer. * **Parasitic Infections:** IgE levels are also characteristically elevated in helminthic infections (e.g., *Ascaris*), where it aids in eosinophil-mediated destruction of the parasite. * **Receptor:** Remember that IgE binds to the **Fc portion** of the antibody to mast cells. * **Casoni’s Test:** An immediate hypersensitivity skin test used for Hydatid disease.

Question 86: Which of the following statements is NOT true about the secondary immunoglobulin response?

A. Predominance of IgG
B. Takes 5 days to appear (Correct Answer)
C. Depends on immunologic memory
D. May be repeated within physiological limits

Explanation: ### Explanation The **secondary immune response** (anamnestic response) occurs when the immune system encounters an antigen for the second or subsequent time. This response is characterized by its speed, intensity, and specificity due to the presence of **memory B-cells**. **Why Option B is the correct answer (The False Statement):** The secondary response is significantly faster than the primary response. While the primary response has a long lag phase of 5–10 days, the secondary response has a very short lag phase, typically appearing within **1–3 days**. Therefore, stating it takes 5 days to appear is incorrect in the context of a secondary response. **Analysis of Incorrect Options:** * **Option A (Predominance of IgG):** This is true. While the primary response is dominated by IgM, the secondary response involves "class switching," leading to a predominance of **IgG** (and sometimes IgA or IgE) with higher affinity for the antigen. * **Option C (Depends on immunologic memory):** This is true. The rapid mobilization is entirely dependent on memory B and T cells generated during the initial exposure. * **Option D (May be repeated):** This is true. The secondary response can be triggered multiple times upon re-exposure to the same pathogen, which is the fundamental principle behind **booster doses** in vaccination. ### NEET-PG High-Yield Pearls * **Lag Phase:** Primary (5–10 days) vs. Secondary (1–3 days). * **Antibody Titer:** Much higher and persists longer in the secondary response. * **Affinity Maturation:** Antibodies produced in the secondary response have a higher binding affinity for the antigen compared to the primary response. * **Antigens:** Primary response is elicited by both T-dependent and T-independent antigens; the secondary response is typically elicited by **T-dependent antigens**.

Question 87: Which of the following is associated with HLA-B27?

A. Autoimmune diseases
B. Graft rejection
C. Cell-mediated cytolysis of virally infected cells
D. Mixed leukocyte reaction (Correct Answer)

Explanation: **Explanation:** **HLA-B27** is a Class I Major Histocompatibility Complex (MHC) molecule. The correct answer is **Mixed Leukocyte Reaction (MLR)** because this laboratory test measures the proliferative response of T-lymphocytes when they encounter foreign MHC antigens (both Class I and Class II) on the surface of donor cells. Since HLA-B27 is a specific MHC allele, it acts as an alloantigen that triggers this reaction during cross-matching. **Analysis of Options:** * **Option D (Correct):** MLR is an *in vitro* model of T-cell recognition. When cells expressing HLA-B27 are mixed with lymphocytes from an individual lacking this allele, the T-cells recognize the HLA-B27 molecule as "non-self," leading to blast transformation and DNA synthesis. * **Option A:** While HLA-B27 is strongly *linked* to certain autoimmune conditions (like Ankylosing Spondylitis), it is not a general mechanism for all autoimmune diseases. Most systemic autoimmune diseases (like SLE) are more commonly associated with HLA-DR (Class II). * **Option B:** Graft rejection is a clinical process mediated by multiple HLA loci (A, B, C, and DR). While HLA-B27 can contribute, it is not uniquely "associated" with the process more than any other HLA molecule. * **Option C:** This describes the general function of **MHC Class I** molecules. While HLA-B27 performs this role, the question asks for a specific association. In the context of standardized exams, MLR is the classic functional assay used to identify HLA compatibility. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic (PAIR):** HLA-B27 is associated with **P**soriatic arthritis, **A**nkylosing spondylitis (90% association), **I**nflammatory bowel disease, and **R**eactive arthritis. * **MHC Class I (A, B, C):** Present endogenous antigens to **CD8+ T-cells**. * **MHC Class II (DR, DQ, DP):** Present exogenous antigens to **CD4+ T-cells**. * **MLR** is primarily used to determine compatibility before hematopoietic stem cell transplantation.

Question 88: A 38-year-old woman presents with fever of 103°F, hypotension, confusion, and a diffuse, erythematous rash. She had uncontrollable epistaxis for which a nasal pack was placed 3 days ago. What is the likely mechanism of action of the microbial toxin that has caused her current illness?

A. Increased antigen presentation by macrophages
B. Polyclonal activation of T-cells (Correct Answer)
C. Uncontrolled activation of complement
D. Enhancement of phagocytosis

Explanation: ### Explanation **Clinical Diagnosis: Toxic Shock Syndrome (TSS)** The patient presents with the classic triad of high fever, hypotension (shock), and a diffuse rash, following the use of a nasal pack. This clinical picture is highly suggestive of **Toxic Shock Syndrome (TSS)**, typically caused by the **Toxic Shock Syndrome Toxin-1 (TSST-1)** produced by *Staphylococcus aureus*. **1. Why Option B is Correct:** TSST-1 belongs to a class of proteins called **Superantigens**. Unlike conventional antigens, superantigens do not undergo intracellular processing. Instead, they bind directly to the **outer surface of the MHC Class II molecule** on Antigen-Presenting Cells (APCs) and the **Variable beta (Vβ) chain of the T-Cell Receptor (TCR)**. This bypasses the specificity of the immune response, leading to the **polyclonal activation of up to 20% of the body’s T-cells**. This results in a massive "cytokine storm" (release of IL-1, IL-2, TNF-α, and IFN-γ), which causes the systemic inflammatory response and shock. **2. Why the Other Options are Incorrect:** * **Option A:** Superantigens actually bypass standard antigen processing and presentation, rather than increasing it. * **Option C:** While complement may be involved in systemic inflammation, the primary driver of TSS is the cytokine storm from T-cell overactivation, not a direct complement defect. * **Option D:** TSST-1 does not enhance phagocytosis; in fact, the overwhelming systemic response often impairs effective immune clearance. **3. High-Yield Clinical Pearls for NEET-PG:** * **Common Scenarios:** Menstrual TSS (highly absorbent tampons) and Non-menstrual TSS (nasal packs, surgical wound infections). * **Key Cytokine:** **TNF-α** is primarily responsible for the hypotension and tissue damage. * **Other Superantigens:** Staphylococcal enterotoxins (food poisoning) and Streptococcal Pyrogenic Exotoxin A (SpeA) causing Streptococcal TSS. * **Binding Site:** Remember the specific binding to the **Vβ region** of the TCR; this is a frequent examiner favorite.

Question 89: Glomerulonephritis is a type of?

A. Type-3 hypersensitivity (Correct Answer)
B. Type-1 hypersensitivity
C. Type-2 hypersensitivity
D. Type-4 hypersensitivity

Explanation: **Explanation:** **Glomerulonephritis** (specifically Post-Streptococcal Glomerulonephritis or PSGN) is a classic example of **Type-3 Hypersensitivity**, which is mediated by **Immune Complexes**. 1. **Why Type-3 is Correct:** In Type-3 reactions, soluble antigens bind with antibodies (IgG or IgM) to form antigen-antibody complexes. These complexes circulate in the blood and eventually deposit in tissues—in this case, the **glomerular basement membrane**. Once deposited, they activate the **complement system** (classical pathway), leading to the recruitment of neutrophils, release of lysosomal enzymes, and subsequent tissue damage (inflammation of the glomeruli). 2. **Why Other Options are Incorrect:** * **Type-1 (Immediate):** Mediated by **IgE** and mast cell degranulation (e.g., Anaphylaxis, Asthma). It does not involve immune complex deposition in the kidneys. * **Type-2 (Cytotoxic):** Involves antibodies binding directly to antigens on **cell surfaces** or fixed tissues (e.g., Goodpasture syndrome, where antibodies attack the GBM directly). While some forms of GN are Type-2, the standard "Glomerulonephritis" referred to in general exams is the immune-complex mediated Type-3. * **Type-4 (Delayed):** Mediated by **T-cells**, not antibodies (e.g., Mantoux test, Contact dermatitis). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Type-3:** **S**ystemic Lupus Erythematosus (SLE), **S**erum Sickness, **S**treptococcal GN (PSGN), and **A**rthus reaction (The "3 Ss and an A"). * **Complement Levels:** In Type-3 reactions like PSGN, serum **C3 levels are characteristically low** because the complement is "consumed" during the inflammatory process. * **Immunofluorescence:** Type-3 GN shows a **"Lumpy-Bumpy"** or granular appearance, whereas Type-2 (Goodpasture) shows a **Linear** pattern.

Question 90: Which of the following are large, granular lymphoid cells that are mediators of antibody-dependent cellular cytotoxicity?

A. macrophages
B. natural killer (NK) cells (Correct Answer)
C. T lymphocytes, suppressor subset
D. B lymphocytes

Explanation: **Explanation:** The correct answer is **Natural Killer (NK) cells**. NK cells are a distinct lineage of lymphocytes that do not express antigen-specific receptors (TCR or BCR). Morphologically, they are identified as **Large Granular Lymphocytes (LGLs)** due to the presence of prominent azurophilic cytoplasmic granules containing perforins and granzymes. NK cells mediate **Antibody-Dependent Cellular Cytotoxicity (ADCC)** through their surface receptor **CD16** (FcγRIII). This receptor binds to the Fc portion of IgG antibodies already attached to a target cell (e.g., a virus-infected or tumor cell). Once bound, the NK cell releases its granules, inducing apoptosis in the target cell. **Analysis of Incorrect Options:** * **A. Macrophages:** While they can participate in ADCC and are phagocytic, they are myeloid in origin, not lymphoid, and are not classified as "large granular lymphocytes." * **C. T lymphocytes (Suppressor subset/CD8+):** While CD8+ T cells are lymphoid and contain granules, they are "Small Lymphocytes" in their resting state and primarily recognize antigens via MHC Class I, not via Fc receptors for ADCC. * **D. B lymphocytes:** These are small, non-granular lymphocytes responsible for humoral immunity (antibody production). They do not have cytotoxic killing capabilities. **NEET-PG High-Yield Pearls:** * **Markers:** NK cells are typically **CD16+ and CD56+**, but **CD3 negative**. * **MHC Independence:** Unlike T-cells, NK cells kill cells that have "missing self" (downregulated MHC-I expression), a common evasion tactic by viruses and tumors. * **Cytokine Production:** They are a major source of **IFN-gamma**, which activates macrophages.

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