Immunology Practice Questions

Q: Lysozyme is present in which of the following body secretions?

Cerebrospinal fluid (CSF). **Explanation:** Lysozyme (also known as muramidase) is a key component of the **innate immune system**. It functions as an antibacterial enzyme by hydrolyzing the $\beta$-(1,4)-glycosidic bonds between N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM) in the **peptidoglycan** layer of bacterial cell walls, particularly in Gram-positive bacteria. **Why the Correct Answer is CSF:** In a healthy physiological state, lysozyme is notably **absent** or present in only negligible traces in the **Cerebrospinal Fluid (CSF)**, sweat, and urine. Therefore, in the context of standard medical examinations, CSF is frequently cited as the secretion lacking lysozyme. **Analysis of Options:** * **A. Lacrimal secretions (Tears):** These contain high concentrations of lysozyme to protect the ocular surface from bacterial colonization. * **C. Saliva:** Lysozyme is a primary antibacterial agent in the oral cavity, working alongside lactoferrin and IgA. * **D. Respiratory tract secretions:** Mucus in the nasopharynx and bronchial tree contains lysozyme to trap and degrade inhaled pathogens. **Clinical Pearls for NEET-PG:** * **Diagnostic Marker:** While normally absent in CSF, lysozyme levels **increase** significantly in cases of **bacterial meningitis**, making it a useful biochemical marker to differentiate it from viral meningitis. * **Cellular Source:** It is primarily synthesized by **monocytes, macrophages, and neutrophils**. * **Sarcoidosis:** Elevated serum lysozyme levels can be seen in sarcoidosis and certain monocytic leukemias (AML-M4 and M5). * **Gram-Negative Resistance:** Lysozyme is less effective against Gram-negative bacteria because their peptidoglycan layer is protected by an outer lipopolysaccharide membrane.

Q: What is the C3 convertase in the alternative complement pathway?

C3bBb. ### Explanation The complement system is a crucial component of innate immunity, consisting of a cascade of proteins that lead to opsonization, inflammation, and cell lysis. **Correct Answer: C. C3bBb** In the **Alternative Pathway**, activation begins with the spontaneous hydrolysis of C3 ("tick-over"). When C3b binds to a pathogen surface, it recruits **Factor B**. Factor B is then cleaved by **Factor D** into Ba and Bb. The resulting complex, **C3bBb**, acts as the **C3 convertase**, which further cleaves more C3 into C3a and C3b, creating a powerful amplification loop. **Analysis of Incorrect Options:** * **A. C4b2b:** This is the C3 convertase for the **Classical** and **Lectin** pathways. It is formed after C1 (Classical) or MASP (Lectin) cleaves C4 and C2. * **B. C3b:** While C3b is a component of the convertase and acts as a potent **opsonin**, it lacks enzymatic activity on its own to cleave C3. * **C. C3a:** This is a small peptide fragment released after C3 cleavage. It functions as an **anaphylatoxin**, triggering mast cell degranulation and inflammation. **High-Yield Facts for NEET-PG:** * **Properdin (Factor P):** This is the only known positive regulator of complement; it stabilizes the C3bBb complex, increasing its half-life. * **C5 Convertase:** In the alternative pathway, adding another C3b to the C3 convertase forms **C3bBb3b** (the C5 convertase). * **Membrane Attack Complex (MAC):** All pathways converge at the formation of the MAC (**C5b-C9**). * **Deficiency:** Deficiency of early alternative pathway components (e.g., Properdin, Factor D) increases susceptibility to *Neisseria* infections.

Q: Which one of the following antibodies is produced rapidly and in high amounts during a secondary immune response?

IgG. ### Explanation The correct answer is **IgG**. **1. Why IgG is correct:** The secondary immune response (anamnestic response) occurs when the immune system encounters an antigen for the second or subsequent time. This response is mediated by **Memory B-cells**. Upon re-exposure, these cells rapidly proliferate and undergo **class switching**, leading to the production of high titers of **IgG**. Compared to the primary response, the secondary response has a shorter lag phase, a faster rate of antibody rise, and reaches a much higher peak concentration. Furthermore, the antibodies produced have a higher affinity for the antigen (affinity maturation). **2. Why the other options are incorrect:** * **IgM:** This is the first antibody produced during the **primary immune response**. In a secondary response, IgM is produced in low amounts or remains similar to primary levels, while IgG dominates. * **IgA:** This is the primary secretory antibody found in mucosal surfaces (tears, saliva, colostrum). While it can be part of a secondary response in mucosal immunity, IgG is the systemic hallmark of secondary humoral immunity. * **IgM and IgG:** While both are present, they are not produced in equal "high amounts" rapidly. The defining characteristic of the secondary response is the massive shift toward IgG. **3. NEET-PG High-Yield Pearls:** * **Primary Response:** Long lag phase (5–10 days), predominantly **IgM**, lower antibody titer. * **Secondary Response:** Short lag phase (1–3 days), predominantly **IgG**, much higher titer, persists longer. * **Affinity Maturation:** This process occurs during the secondary response, making the IgG "fit" the antigen better than the initial IgM. * **Placental Transfer:** IgG is the only antibody that crosses the placenta, providing passive immunity to the fetus.

Q: Which of the following is a superantigen?

Exfoliative toxin of Staphylococcus. ### Explanation **Correct Answer: A. Exfoliative toxin of Staphylococcus** **Understanding Superantigens:** Superantigens (SAgs) are potent immunostimulatory molecules that bypass the standard antigen-processing pathway. Unlike conventional antigens, which are processed and presented in the MHC-II groove, superantigens bind **directly and non-specifically** to the **outer surface of the MHC-II molecule** on Antigen Presenting Cells (APCs) and the **Vβ region of the T-cell receptor (TCR)**. This results in the massive activation of up to 20% of the body’s T-cells, leading to a "cytokine storm" (IFN-γ, IL-1, IL-6, TNF-α). **Staphylococcal Exfoliative toxins (ETA, ETB)**, responsible for Staphylococcal Scalded Skin Syndrome (SSSS), function as superantigens. **Analysis of Incorrect Options:** * **B. Lipopolysaccharide (LPS):** LPS is a classic **Endotoxin** found in the outer membrane of Gram-negative bacteria. It activates the innate immune system via TLR-4 but does not act as a T-cell superantigen. * **C. Enterotoxin of V. cholerae:** This is an **A-B subunit toxin** that acts by ADP-ribosylation of Gs proteins, leading to increased cAMP and secretory diarrhea. It is not a superantigen. * **D. Shiga toxin of EHEC:** This is also an **A-B toxin** that inhibits protein synthesis by damaging the 28S ribosomal RNA. It is associated with Hemolytic Uremic Syndrome (HUS). **High-Yield Clinical Pearls for NEET-PG:** * **Common Superantigens:** * *Staphylococcus aureus:* TSST-1 (Toxic Shock Syndrome), Enterotoxins (Food poisoning), Exfoliative toxin. * *Streptococcus pyogenes:* Erythrogenic toxin (SpeA and SpeC). * **Key Feature:** They do **not** require processing by APCs and bind to the **Vβ region** of TCR. * **Clinical Result:** Massive release of **TNF-α and IL-1**, leading to shock and multi-organ failure.

Q: Which of the following statements is true about interferon?

It inhibits viral replication in cells.. ### Explanation **Correct Option: B. It inhibits viral replication in cells.** Interferons (IFNs) are natural glycoproteins produced by host cells in response to viral infections. They do not kill viruses directly; instead, they act as signaling molecules. When a cell is infected, it secretes IFNs which bind to receptors on neighboring uninfected cells. This triggers the synthesis of **antiviral proteins (AVPs)**, such as *2',5'-oligoadenylate synthetase* and *protein kinase R*, which degrade viral mRNA and inhibit protein synthesis, thereby preventing viral replication. **Analysis of Incorrect Options:** * **Option A:** Interferons are **endogenous** biological products (cytokines) produced by the body, not synthetic drugs, although recombinant versions are used therapeutically. * **Option C:** Interferons are **host-specific but not virus-specific**. This means human interferon will work against any virus (Influenza, HBV, etc.) in a human cell, but human interferon is generally ineffective in other species (e.g., mice). **High-Yield NEET-PG Pearls:** * **Classification:** * **Type I (IFN-α, IFN-β):** Primarily antiviral and produced by leucocytes and fibroblasts. * **Type II (IFN-γ):** Produced by Th1 cells/NK cells; primarily an **immunomodulator** (activates macrophages). * **Mechanism:** They induce an "antiviral state" in surrounding cells. * **Clinical Use:** IFN-α is used in the treatment of Chronic Hepatitis B, Hepatitis C, and Kaposi Sarcoma. * **Key Fact:** Interferons are the first line of innate immune defense against viral infections before antibodies appear.

Q: Which surface marker is characteristically present on Natural Killer (NK) cells?

CD 16. **Explanation:** **Natural Killer (NK) cells** are large granular lymphocytes that form a crucial part of the innate immune system. They are characteristically identified by the presence of **CD16** and **CD56**, while notably lacking the T-cell receptor (CD3). **Why CD16 is the Correct Answer:** CD16 is the **FcγRIII** (low-affinity receptor for the Fc portion of IgG). Its presence on NK cells is functional: it allows these cells to bind to antibody-coated target cells, triggering **Antibody-Dependent Cellular Cytotoxicity (ADCC)**. This is a high-yield mechanism where NK cells release perforins and granzymes to destroy virally infected or tumor cells. **Analysis of Incorrect Options:** * **CD44:** A cell-surface glycoprotein involved in cell-cell interactions, cell adhesion, and migration (notably a receptor for hyaluronic acid). It is not a specific marker for NK cells. * **CD54 (ICAM-1):** An intercellular adhesion molecule expressed on endothelial cells and immune cells. It binds to LFA-1 and is involved in leukocyte extravasation during inflammation. * **CD32 (FcγRII):** An Fc receptor found primarily on B cells, macrophages, and neutrophils. It acts as an inhibitory receptor on B cells to regulate antibody production. **High-Yield Clinical Pearls for NEET-PG:** * **NK Cell Markers:** CD16 (ADCC) and CD56 (NCAM - Neural Cell Adhesion Molecule). * **Defining Feature:** NK cells are **CD3 negative**. If a cell is CD3+ and CD56+, it is an NKT cell. * **Function:** They provide the first line of defense against intracellular pathogens and tumors by recognizing the **absence of MHC Class I** molecules (the "Missing Self" hypothesis). * **Cytokine Activation:** NK cell activity is significantly enhanced by **IL-2 and IL-12**.

Q: A 35-year-old male patient presents with numerous subcutaneous hemorrhages. History and physical examination reveal that he has been taking sedormid (a sedative) for the past week. Laboratory tests indicate normal hemoglobin and white blood cell levels with significant thrombocytopenia. You suspect that he has developed a drug-induced type II hypersensitivity reaction. This reaction may occur if the drug acts as which of the following?

Acts as a hapten. **Explanation** The clinical presentation of subcutaneous hemorrhages (purpura) and isolated thrombocytopenia following drug intake (Sedormid) is a classic example of **Drug-Induced Immune Thrombocytopenia**, a **Type II Hypersensitivity reaction**. **Why Option B is Correct:** Drugs like Sedormid, penicillin, or quinidine are small molecules (low molecular weight) that are not immunogenic on their own. They act as **haptens**. In this specific reaction, the drug binds to the surface of platelets (the carrier protein). This drug-platelet complex becomes immunogenic, stimulating the production of antibodies (IgG or IgM). These antibodies bind to the drug-coated platelets, leading to their destruction via the **complement system** (classical pathway) or **opsonization** (phagocytosis by splenic macrophages), resulting in thrombocytopenia. **Why Incorrect Options are Wrong:** * **Option A:** Activation of T-cytotoxic cells is characteristic of **Type IV (Delayed) Hypersensitivity**, not Type II. * **Option C:** Mast cell degranulation and mediator release (histamine) are the hallmarks of **Type I (Immediate) Hypersensitivity**, typically seen in anaphylaxis or urticaria. * **Option D:** Respiratory burst and oxygen radical production are primary mechanisms used by neutrophils and macrophages to kill phagocytosed bacteria, not the primary mechanism of drug-induced platelet destruction. **High-Yield Clinical Pearls for NEET-PG:** * **Type II Hypersensitivity** is "Antibody-Mediated" (Cytotoxic). * **Common Examples:** Erythroblastosis fetalis, Rheumatic fever, Goodpasture syndrome, Myasthenia gravis, and Graves' disease. * **Hapten Rule:** A hapten is a substance that is **antigenic** (can react with antibodies) but not **immunogenic** (cannot elicit an immune response) unless conjugated to a carrier protein.

Q: Which of the following cells do not typically present MHC class II molecules?

Eosinophils. **Explanation:** The core concept tested here is the distribution of **Major Histocompatibility Complex (MHC) Class II** molecules. Unlike MHC Class I, which is expressed on all nucleated cells, MHC Class II is constitutively expressed only on **Professional Antigen-Presenting Cells (pAPCs)**. These cells are essential for activating CD4+ T-helper cells. **Why Eosinophils are the Correct Answer:** Eosinophils are primarily granulocytes involved in parasitic infections and allergic responses. While they can be induced to express MHC II under specific inflammatory conditions, they are **not** considered typical or professional APCs. In the context of standard immunology and NEET-PG questions, granulocytes (Neutrophils, Eosinophils, Basophils) are categorized as cells that do not typically present MHC II. **Analysis of Incorrect Options:** * **Dendritic Cells:** These are the most potent professional APCs. They are the only cells capable of activating naive T-cells. * **Macrophages:** These are professional APCs that present phagocytosed antigens to effector T-cells at the site of infection. * **Lymphocytes (specifically B-cells):** B-lymphocytes are professional APCs. They internalize antigens via surface immunoglobulins and present them to T-helper cells to receive signals for isotype switching and memory cell formation. **High-Yield Clinical Pearls for NEET-PG:** * **MHC II Distribution:** Professional APCs = **B**-cells, **D**endritic cells, and **M**acrophages (Mnemonic: **BDM**). * **MHC Restriction:** MHC Class I interacts with **CD8+** T-cells (1 × 8 = 8), while MHC Class II interacts with **CD4+** T-cells (2 × 4 = 8). * **Non-Professional APCs:** Under the influence of **IFN-gamma**, certain non-professional cells (like vascular endothelial cells or thyroid epithelial cells) can transiently express MHC II.

Question 1

Lysozyme is present in which of the following body secretions?

Accepted Answer

Cerebrospinal fluid (CSF)

Answer

Lacrimal secretions

Answer

Saliva

Answer

Respiratory tract secretions

Question 2

What is the C3 convertase in the alternative complement pathway?

Accepted Answer

C3bBb

Answer

C4b2b

Answer

C3b

Answer

C3a

Question 3

Which one of the following antibodies is produced rapidly and in high amounts during a secondary immune response?

Accepted Answer

IgG

Answer

IgA

Answer

IgM

Answer

IgM and IgG

Question 4

Which of the following is a superantigen?

Accepted Answer

Exfoliative toxin of Staphylococcus

Answer

Lipopolysaccharide of Gram-negative bacteria

Answer

Enterotoxin of V. cholerae

Answer

Shiga toxin of EHEC

Question 5

Which of the following statements is true about interferon?

Accepted Answer

It inhibits viral replication in cells.

Answer

It is a synthetic antiviral agent.

Answer

It is specific for a particular virus.

Answer

None of the above.

Question 6

Which surface marker is characteristically present on Natural Killer (NK) cells?

Accepted Answer

CD 16

Answer

CD 44

Answer

CD 54

Answer

CD 32

Question 7

A 35-year-old male patient presents with numerous subcutaneous hemorrhages. History and physical examination reveal that he has been taking sedormid (a sedative) for the past week. Laboratory tests indicate normal hemoglobin and white blood cell levels with significant thrombocytopenia. You suspect that he has developed a drug-induced type II hypersensitivity reaction. This reaction may occur if the drug acts as which of the following?

Accepted Answer

Acts as a hapten

Answer

Activates T cytotoxic cells

Answer

Induces mast cell degranulation, releasing mediators such as histamine, leukotrienes, and prostaglandins

Answer

Induces oxygen radical production through the respiratory burst pathway

Question 8

Which of the following cells do not typically present MHC class II molecules?

Accepted Answer

Eosinophils

Answer

Macrophage

Answer

Dendritic cells

Answer

Lymphocytes

Question 9

The Ouchterlony procedure is a type of immunodiffusion characterized by which of the following?

Accepted Answer

Double diffusion in two dimensions

Answer

Single diffusion in one dimension

Answer

Double diffusion in one dimension

Answer

Single diffusion in two dimensions

Question 10

Which of the following is characteristic of the mucosal immune system?

Accepted Answer

Tolerance to foreign antigens is the norm rather than the exception

Answer

A vigorous response is made to all nonself antigens encountered

Answer

Chronic inflammation makes an inhospitable environment for microbes

Answer

IL-2 and IFN-g contribute to a Th-1 like environment

Immunology — MCQs

Immunology — MCQs

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