Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 681: All of the following statements regarding hypersensitivity reactions are true, except:

A. Erythema nodosum leprosum is a Type III hypersensitivity reaction.
B. Post-streptococcal glomerulonephritis is a Type III hypersensitivity reaction.
C. The Schick test is an example of delayed hypersensitivity. (Correct Answer)
D. Mismatched blood transfusion is a Type II hypersensitivity reaction.

Explanation: ### Explanation The correct answer is **C**. The **Schick test** is not an example of delayed hypersensitivity; rather, it is a **neutralization test** used to determine susceptibility to *Corynebacterium diphtheriae*. In this test, diphtheria toxin is injected intradermally. If the person lacks antibodies (non-immune), the toxin causes local inflammation (positive result). If antibodies are present, they neutralize the toxin, and no reaction occurs. **Analysis of other options:** * **Option A (Erythema Nodosum Leprosum):** This is a classic example of **Type III hypersensitivity** (Arthus-type). It occurs due to the deposition of immune complexes (antigen-antibody) in tissues, typically during the treatment of lepromatous leprosy. * **Option B (Post-streptococcal Glomerulonephritis):** This is a **Type III hypersensitivity** reaction where circulating immune complexes (formed against Group A Streptococcus) deposit in the glomerular basement membrane, leading to inflammation. * **Option D (Mismatched Blood Transfusion):** This is a **Type II hypersensitivity** (Cytotoxic) reaction. Pre-formed antibodies (IgM/IgG) bind to antigens on the transfused RBCs, leading to complement activation and cell lysis. **High-Yield Clinical Pearls for NEET-PG:** * **Type IV (Delayed) Hypersensitivity Examples:** Mantoux test (Tuberculin), Lepromin test, Mitsuda reaction, Contact dermatitis, and Graft rejection. * **Type III Examples:** SLE, Rheumatoid Arthritis, Serum Sickness, and Farmer’s Lung. * **Type II Examples:** Myasthenia gravis, Graves' disease, Goodpasture syndrome, and Rheumatic fever. * **Mnemonic for Hypersensitivity (Gell & Coombs):** **ACID** (**A**naphylactic - I, **C**ytotoxic - II, **I**mmune Complex - III, **D**elayed - IV).

Question 682: Which of the following is a flocculation test?

A. Widal test
B. Weil-Felix test
C. VDRL (Correct Answer)
D. Paul-Bunnel test

Explanation: ### Explanation **VDRL (Venereal Disease Research Laboratory)** is the correct answer because it is a classic example of a **Slide Flocculation Test**. #### 1. Why VDRL is the Correct Answer Flocculation is a specific type of precipitation reaction where the antigen is **particulate** (rather than soluble). In the VDRL test, the antigen (cardiolipin-cholesterol-lecithin) remains in a fine suspension. When it reacts with the patient's antibodies (reagin), the particles clump together to form visible **flakes or "floccules"** instead of a sediment. This reaction must be viewed under a light microscope. #### 2. Why Other Options are Incorrect * **Widal Test (Option A):** This is a **Tube/Slide Agglutination** test used for Enteric fever. It involves the clumping of whole bacterial cells (Salmonella Typhi/Paratyphi). * **Weil-Felix Test (Option B):** This is a **Heterophile Agglutination** test. It uses *Proteus* antigens to detect antibodies against Rickettsial diseases. * **Paul-Bunnel Test (Option C):** This is also a **Heterophile Agglutination** test used to diagnose Infectious Mononucleosis (EBV), where the patient's antibodies agglutinate sheep RBCs. #### 3. Clinical Pearls for NEET-PG * **VDRL vs. RPR:** VDRL is a slide flocculation test requiring a microscope, whereas **RPR (Rapid Plasma Reagin)** is a macroscopic flocculation test (uses charcoal particles) visible to the naked eye. * **Screening vs. Confirmatory:** VDRL/RPR are non-specific screening tests for Syphilis. Positive results must be confirmed with specific treponemal tests like **FTA-ABS** or **TPHA**. * **Prozone Phenomenon:** A false negative VDRL can occur due to very high antibody titers (Prozone), common in secondary syphilis. * **Other Flocculation Tests:** Kahn test (Tube flocculation).

Question 683: Which codon would tRNArmet recognize?

A. AUG (Correct Answer)
B. UGC
C. GUG
D. GCU

Explanation: **Explanation:** In protein synthesis, the initiation of translation is a highly specific process. The correct answer is **AUG** because it is the universal **start codon** (initiator codon) that codes for Methionine. 1. **Why AUG is correct:** In eukaryotes and prokaryotes, translation begins at the AUG codon on mRNA. This codon is recognized by a specific initiator tRNA, denoted as **tRNAiMet** (or **tRNAfMet** in bacteria/mitochondria). This tRNA carries Methionine (or N-formylmethionine) to the P-site of the ribosome to kickstart the polypeptide chain. 2. **Why other options are incorrect:** * **UGC:** Codes for Cysteine. * **GUG:** Usually codes for Valine. While it can rarely act as an alternative start codon in some prokaryotes, it is not the primary recognition site for tRNAiMet. * **GCU:** Codes for Alanine. **High-Yield Clinical Pearls for NEET-PG:** * **Prokaryotes vs. Eukaryotes:** In bacteria, the initiator amino acid is **N-formylmethionine (fMet)**. fMet is a potent chemoattractant for neutrophils, which is why bacterial infections trigger a rapid inflammatory response. * **Kozak Sequence:** In eukaryotes, the efficiency of AUG recognition is increased by the surrounding **Kozak consensus sequence** (5’-ACCAUGG-3’). * **Shine-Dalgarno Sequence:** In prokaryotes, the 16S rRNA binds to this purine-rich sequence upstream of the AUG to align the ribosome correctly. * **Stop Codons:** Remember the three "nonsense" or stop codons that do not code for any amino acid: **UAA, UAG, and UGA**.

Question 684: Type 5 hypersensitivity reaction is a modification of?

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

Explanation: **Explanation:** **Type 5 hypersensitivity** (also known as Stimulatory Hypersensitivity) is considered a modification of **Type 2 hypersensitivity** because both involve antibodies (IgG or IgM) binding directly to antigens on the cell surface. * **Why Type 2 is correct:** In classic Type 2 reactions, antibodies lead to cell destruction (via complement or phagocytosis). In Type 5, the antibodies do not destroy the cell; instead, they bind to cell-surface receptors and **mimic the action of natural ligands**, leading to overstimulation of the cell's function. Because the mechanism involves site-specific antibody-antigen binding, it is classified as a subtype of Type 2. * **Why others are incorrect:** * **Type 1:** Involves IgE-mediated mast cell degranulation (Allergy/Anaphylaxis). * **Type 3:** Involves the deposition of circulating **Antigen-Antibody complexes** in tissues, not direct binding to cell-surface receptors. * **Type 4:** Is a **delayed-type** reaction mediated by T-cells, not antibodies. **Clinical Pearls for NEET-PG:** 1. **Classic Example:** **Graves’ Disease**. Here, Long-Acting Thyroid Stimulators (LATS) / Thyroid Stimulating Immunoglobulins (TSI) bind to TSH receptors, stimulating excess thyroid hormone production. 2. **Another Example:** **Myasthenia Gravis** (though often grouped under Type 2, it involves antibodies blocking/internalizing ACh receptors). 3. **Key Distinction:** If the question asks for the mechanism of Graves' disease and Type 5 is not an option, always choose **Type 2**. 4. **Coombs Classification:** The original Gell and Coombs classification described four types; Type 5 was added later as a specialized variant of Type 2.

Question 685: Delayed hypersensitivity reaction is mediated by which type of lymphocyte?

A. B lymphocyte
B. NK cell
C. Mast cell
D. T lymphocyte (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. T lymphocyte** **Mechanism:** Delayed-type hypersensitivity (DTH), or **Type IV hypersensitivity**, is the only hypersensitivity reaction that is **cell-mediated** rather than antibody-mediated. It is primarily driven by **T lymphocytes** (specifically Th1 cells and CD8+ T cells). Upon re-exposure to an antigen, sensitized T cells release cytokines (like IFN-γ and TNF-α), which recruit and activate macrophages, leading to tissue inflammation and damage. The reaction is termed "delayed" because it typically takes **48–72 hours** to manifest, reflecting the time required for T cell recruitment and cytokine production. **Analysis of Incorrect Options:** * **A. B lymphocyte:** B cells are responsible for humoral immunity and antibody production. They mediate Type I, II, and III hypersensitivity reactions via IgE, IgG, or IgM. * **B. NK cell:** Natural Killer cells are part of the innate immune system. While they play a role in antibody-dependent cellular cytotoxicity (ADCC), they are not the primary mediators of DTH. * **C. Mast cell:** Mast cells are the primary effectors of **Type I (Immediate) hypersensitivity**. They degranulate and release histamine upon the cross-linking of surface-bound IgE by an allergen. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Examples:** Mantoux (Tuberculin) test, Contact dermatitis (e.g., Poison ivy, Nickel allergy), Lepromin test, and Graft rejection. * **Key Cytokine:** **Interferon-gamma (IFN-γ)** is the most important cytokine for activating macrophages in Type IV reactions. * **Histology:** The hallmark of a chronic Type IV reaction is **Granuloma formation** (seen in Tuberculosis and Sarcoidosis). * **Memory Tip:** Remember the **4 "A"s** of Hypersensitivity: Type I (**A**llergy/Atopy), Type II (**A**ntibody), Type III (**A**ntigen-Antibody complex), Type IV (**A**ctivated T cells).

Question 686: Which of the following is NOT a macrophage?

A. Monocyte
B. Microglia
C. Kupffer cells
D. Lymphocytes (Correct Answer)

Explanation: **Explanation:** The question tests your knowledge of the **Mononuclear Phagocyte System (MPS)**, a lineage of cells derived from the bone marrow that are primarily responsible for phagocytosis and antigen presentation. **Why Lymphocytes are the correct answer:** Lymphocytes (T-cells, B-cells, and NK cells) are part of the **adaptive immune system** (except NK cells) and originate from the **lymphoid progenitor lineage**. Unlike macrophages, they are not primarily phagocytic. They function through antibody production or cell-mediated cytotoxicity rather than engulfing and digesting cellular debris. **Analysis of Incorrect Options:** * **Monocytes:** These are the precursor cells found in the peripheral blood. Once they migrate into tissues, they differentiate into specific macrophages. * **Microglia:** These are the specialized, resident macrophages of the **Central Nervous System (CNS)**. * **Kupffer Cells:** These are specialized macrophages located in the **sinusoids of the liver**, responsible for clearing gut-derived toxins and aged erythrocytes. **High-Yield Clinical Pearls for NEET-PG:** * **Tissue-Specific Macrophages (Must-know list):** * **Lungs:** Alveolar macrophages (Dust cells). * **Bone:** Osteoclasts. * **Skin:** Langerhans cells. * **Kidney:** Mesangial cells. * **Placenta:** Hofbauer cells. * **Connective Tissue:** Histiocytes. * **Key Marker:** **CD14** is a specific surface marker for monocytes and macrophages. * **Function:** Macrophages act as a bridge between innate and adaptive immunity by acting as **Antigen Presenting Cells (APCs)** via MHC II molecules.

Question 687: What is atopy in the context of hypersensitivity?

A. Systemic type I hypersensitivity
B. Local type I hypersensitivity (Correct Answer)
C. Systemic type II hypersensitivity
D. Local type II hypersensitivity

Explanation: **Explanation:** **Atopy** refers to a genetic predisposition to develop localized immediate hypersensitivity reactions to common environmental allergens (such as pollen, house dust mites, or animal dander). **1. Why Option B is Correct:** Atopy is a **Local Type I Hypersensitivity** reaction. It is mediated by **IgE antibodies** bound to mast cells in specific target organs. When an allergen is inhaled, ingested, or touches the skin, it triggers mast cell degranulation in that specific area, leading to localized symptoms. Common clinical manifestations include allergic rhinitis (hay fever), bronchial asthma, and atopic dermatitis (eczema). **2. Why Other Options are Incorrect:** * **Option A:** Systemic Type I hypersensitivity refers to **Anaphylaxis**. Unlike atopy, anaphylaxis is a generalized, life-threatening reaction involving multiple organ systems (e.g., hypotension, laryngeal edema) following systemic exposure to an allergen (e.g., bee sting or IV drugs). * **Options C & D:** Type II hypersensitivity involves **cytotoxic antibodies** (IgG/IgM) directed against cell surface antigens (e.g., Rh incompatibility or Myasthenia Gravis). Atopy is strictly a Type I (IgE-mediated) mechanism. **High-Yield Clinical Pearls for NEET-PG:** * **Genetic Link:** Atopy is often associated with a family history and elevated serum IgE levels. * **The "Atopic March":** This describes the progression from atopic dermatitis in infancy to allergic rhinitis and asthma in later childhood. * **Cytokine Profile:** Atopy is driven by **Th2 cells**, which secrete **IL-4** (induces IgE switching), **IL-5** (activates eosinophils), and **IL-13** (stimulates mucus secretion). * **Diagnosis:** Primarily via the **Skin Prick Test** (Wheal and Flare reaction) or RAST (Radioallergosorbent test).

Question 688: Which type of cell secretes Interferon-alpha (IFN-α)?

A. Leukocytes (Correct Answer)
B. Fibroblasts
C. T helper cells
D. Cytotoxic T cells

Explanation: **Explanation:** Interferons (IFNs) are a group of signaling proteins (cytokines) released by host cells in response to viral infections. They are classified into three types based on their receptor specificity and cellular origin. **1. Why Leukocytes is correct:** **Interferon-alpha (IFN-α)**, also known as **Leukocyte Interferon**, is primarily produced by mononuclear phagocytes (monocytes, macrophages) and B-lymphocytes. These cells secrete IFN-α in response to viral stimulation or exposure to double-stranded RNA. Its primary function is to induce an antiviral state in neighboring cells by inhibiting viral protein synthesis. **2. Why the other options are incorrect:** * **Fibroblasts (Option B):** These cells primarily produce **Interferon-beta (IFN-β)**. Together, IFN-α and IFN-β are classified as **Type I Interferons**. * **T helper cells and Cytotoxic T cells (Options C & D):** These are the primary sources of **Interferon-gamma (IFN-γ)**, also known as **Immune Interferon** or **Type II Interferon**. IFN-γ is secreted by activated T-cells and Natural Killer (NK) cells to enhance the microbicidal activity of macrophages and promote Th1 differentiation. **High-Yield Clinical Pearls for NEET-PG:** * **Type I IFNs (α, β):** Acid-stable; primary role is **antiviral** defense. * **Type II IFN (γ):** Acid-labile; primary role is **immunomodulation** (activates macrophages and increases MHC expression). * **Clinical Use:** Recombinant IFN-α is used therapeutically in Chronic Hepatitis B, Hepatitis C, Hairy Cell Leukemia, and Kaposi Sarcoma. * **Mechanism:** IFNs do not kill viruses directly; they induce the production of **ribonuclease L** (degrades viral mRNA) and **protein kinase R** (inhibits protein synthesis).

Question 689: What was the first cell culture vaccine?

A. Human diploid cell (HDC) vaccine (Correct Answer)
B. Low egg passage (LEP) vaccine
C. Purified chick embryo cell (PCEC) vaccine
D. Purified vero cell (PVC) vaccine

Explanation: ### Explanation **Correct Answer: A. Human diploid cell (HDC) vaccine** The **Human Diploid Cell Vaccine (HDCV)**, developed in the 1960s (specifically using the WI-38 and later MRC-5 cell lines), was the **first vaccine produced using cell culture technology**. Before this, vaccines were primarily derived from animal tissues (like sheep brain for the Semple vaccine) or embryonated eggs. The HDCV revolutionized vaccinology by providing a substrate free from foreign animal proteins, significantly reducing the risk of allergic reactions and neuroparalytic complications (like ADEM) associated with older neural tissue vaccines. **Analysis of Incorrect Options:** * **B. Low Egg Passage (LEP) vaccine:** This is a live-attenuated rabies vaccine prepared in **embryonated duck or chicken eggs**, not cell culture. It is used for animal immunization and is not safe for humans. * **C. Purified Chick Embryo Cell (PCEC) vaccine:** This is a modern cell culture vaccine (using primary chick embryo fibroblasts). While highly effective and commonly used today (e.g., Rabipur), it was developed **after** the HDC vaccine. * **D. Purified Vero Cell (PVC) vaccine:** This uses a continuous lineage of monkey kidney epithelial cells. It is a cost-effective alternative to HDCV but was developed in the late 1970s/early 1980s, making it a **later** advancement. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard:** HDCV remains the "Gold Standard" for rabies pre-exposure and post-exposure prophylaxis due to its high immunogenicity and safety. * **Neural Tissue Vaccines (NTV):** The Semple vaccine (sheep brain) is now obsolete due to the high risk of **post-vaccinal encephalomyelitis**. * **Cell Lines:** Remember **WI-38** and **MRC-5** as the specific human diploid cell lines used for vaccines like Rabies, Rubella, and Hepatitis A. * **Route:** Modern cell culture vaccines (HDCV, PCEC, PVRV) can be administered via the **Intramuscular (IM)** or **Intradermal (ID)** route (Thai Red Cross Schedule).

Question 690: Agglutination with 'O' antigen of S. typhi is inhibited by which of the following?

A. Vi antigen (Correct Answer)
B. Flagellar antigen
C. F antigen
D. All of the above

Explanation: **Explanation:** The correct answer is **Vi antigen**. This phenomenon is a classic concept in enteric fever serology known as **antigenic masking**. **1. Why Vi antigen is correct:** The **Vi (Virulence) antigen** is a surface capsular polysaccharide found in *Salmonella typhi*. It is located outermost to the cell wall **O (Somatic) antigen**. When the Vi antigen is present in high concentrations, it physically covers or "masks" the underlying O antigen. Consequently, anti-O antibodies cannot reach the O antigen to cause agglutination. This can lead to a **false-negative Widal test** result. To overcome this in a laboratory setting, the bacterial suspension must be boiled to destroy the heat-labile Vi antigen, thereby exposing the O antigen for testing. **2. Why other options are incorrect:** * **Flagellar (H) antigen:** These are long, thread-like structures extending far beyond the capsule. While they are immunogenic, they do not form a physical barrier over the O antigen and thus do not inhibit O-agglutination. * **F (Fimbrial) antigen:** These are surface appendages used for attachment. Like H antigens, they do not form a continuous layer dense enough to mask the somatic O antigen. **High-Yield Clinical Pearls for NEET-PG:** * **Heat Stability:** O antigen is heat-stable; Vi and H antigens are heat-labile. * **Diagnostic Significance:** Detection of Vi antibodies is not used for diagnosing acute typhoid but is a valuable screening tool for identifying **chronic typhoid carriers**. * **Widal Test:** A positive Widal test typically shows a four-fold rise in titers. O agglutinins appear early (suggesting acute infection), while H agglutinins appear later and persist longer.

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