Immunology Practice Questions

Q: Which statement about IgM antibody is FALSE?

It is monomeric in nature. **Explanation:** **1. Why Option C is the Correct (False) Statement:** IgM is the largest immunoglobulin and primarily exists as a **pentamer** (five monomer units) in its secreted form, held together by a **J-chain** (Joining chain) and disulfide bonds. While IgM is found as a monomer on the surface of B-cells (acting as a B-cell receptor), its characteristic physiological form in serum is pentameric. Therefore, stating it is "monomeric in nature" as a general rule is incorrect. **2. Analysis of Incorrect Options:** * **Option A (Highest Molecular Weight):** True. Due to its pentameric structure, IgM has a molecular weight of approximately **900,000 Daltons (900 kDa)**, making it the "Millionaire Molecule." * **Option B (Highest Sedimentation Coefficient):** True. Because of its large size and mass, it has the highest sedimentation coefficient, typically **19S** (compared to 7S for IgG). * **Option C (Responsible for Agglutination):** True. With **10 theoretical antigen-binding sites** (valency of 10, though effectively 5 due to steric hindrance), IgM is highly efficient at cross-linking particulate antigens, making it the most potent antibody for agglutination and complement fixation. **3. High-Yield Clinical Pearls for NEET-PG:** * **First Responder:** IgM is the first antibody to appear in response to an initial exposure to an antigen (Primary Immune Response). * **Acute Infection Marker:** Presence of specific IgM in serum indicates a **recent/acute infection** or congenital infection (as IgM cannot cross the placenta). * **Evolutionary Fact:** It is the oldest class of immunoglobulins phylogenetically. * **Intravascular Distribution:** Due to its large size, it is largely confined to the intravascular compartment (80%).

Q: Which components of innate immunity are active against viral cells?

NK cells. **Explanation:** The core of this question lies in distinguishing between **innate** and **adaptive** immunity. **Why NK cells are correct:** Natural Killer (NK) cells are a critical component of the **innate immune system**. Unlike T or B cells, they do not require prior sensitization or MHC-restricted antigen presentation to function. They are specifically designed to target virally infected cells and tumor cells. NK cells detect "missing self" (downregulation of MHC-I molecules, a common viral evasion strategy) and release perforins and granzymes to induce apoptosis in the target cell. They also secrete Interferon-gamma (IFN-γ) to activate macrophages. **Why the other options are incorrect:** * **Cytotoxic T cells (CD8+):** While these are highly effective against viruses, they belong to the **adaptive immune system**. They require specific antigen presentation via MHC-I and take time to proliferate during a primary infection. * **B cells:** These are part of the **adaptive humoral immunity**. Their primary role is to differentiate into plasma cells that produce antibodies. * **Memory B cells:** These are specialized adaptive immune cells formed after an initial infection to provide rapid, long-term protection upon re-exposure. **High-Yield NEET-PG Pearls:** * **NK Cell Markers:** CD16 (FcγRIII, binds IgG for ADCC) and CD56 (NCAM) are the definitive markers. * **ADCC:** NK cells participate in Antibody-Dependent Cellular Cytotoxicity via the CD16 receptor. * **Cytokine Link:** IL-12 and IL-15 are potent activators of NK cells. * **MHC-I:** NK cells are *inhibited* by the presence of normal MHC-I; viruses that downregulate MHC-I to hide from T cells become primary targets for NK cells.

Q: When an antigen is administered for the first time to an animal or a human being who has never been exposed to it, what is the first antibody to develop?

IgM type. **Explanation:** In the **Primary Immune Response**, which occurs when the body encounters a specific antigen for the first time, there is a characteristic sequence of antibody production. After a latent period (lag phase) of 5–10 days, **IgM** is the first class of immunoglobulin to appear. This is because IgM is the "default" antibody produced by naive B cells before they undergo **class-switching**. IgM is a pentamer, providing high avidity to neutralize pathogens early in the infection. **Analysis of Options:** * **Option A (IgG):** IgG is the predominant antibody in the **Secondary Immune Response** (anamnestic response). While it follows IgM in the primary response after class-switching, it is not the *first* to develop. IgG is the only antibody that crosses the placenta. * **Option C (IgA):** This is the primary secretory antibody found in colostrum, saliva, and mucosal surfaces. It provides local immunity but is not the primary systemic responder to a new antigen. * **Option D (IgE):** This antibody is primarily involved in Type I hypersensitivity (allergic) reactions and defense against helminthic parasitic infections. **High-Yield NEET-PG Pearls:** * **IgM:** Largest antibody (Macroglobulin), first to appear in evolution and phylogeny, and indicates **acute/recent infection**. It does not cross the placenta; thus, its presence in a newborn indicates intrauterine infection (e.g., TORCH). * **Lag Phase:** Shorter in secondary response (1–3 days) compared to primary response (5–10 days). * **Affinity Maturation:** Occurs during the transition from IgM to IgG, leading to higher antigen-binding strength in subsequent exposures.

Q: Antisnake venom may cause which type of hypersensitivity reaction?

Type III hypersensitivity reactions. **Explanation:** **Antisnake venom (ASV)** is a classic example of **Type III hypersensitivity**, specifically manifesting as **Serum Sickness**. 1. **Why Type III is correct:** ASV is a form of passive immunization containing foreign (usually equine/horse) proteins. When injected, the body recognizes these proteins as antigens and produces antibodies (IgG/IgM). These antibodies bind to the circulating foreign proteins, forming **soluble immune complexes**. These complexes deposit in small blood vessel walls, basement membranes of joints, and kidneys, activating the complement system and causing systemic inflammation (fever, rash, arthralgia, and proteinuria). 2. **Why other options are incorrect:** * **Type II (Cytotoxic):** Involves antibodies (IgG/IgM) binding directly to antigens on **cell surfaces** or tissues (e.g., Rh incompatibility), not soluble circulating complexes. * **Type IV (Delayed-type):** This is **cell-mediated** (T-cells), occurring 48–72 hours after exposure (e.g., Mantoux test). ASV reactions are antibody-mediated. * **Type V:** Often considered a subtype of Type II, involving stimulatory antibodies (e.g., Graves' disease). **High-Yield Clinical Pearls for NEET-PG:** * **Serum Sickness** is the systemic form of Type III hypersensitivity; **Arthus Reaction** is the localized form. * **Other causes of Type III:** SLE, Post-streptococcal glomerulonephritis (PSGN), and Farmer’s lung. * **Timeline:** Serum sickness typically occurs 7–12 days after administration of the foreign serum. * **Complement levels:** Characteristically, **C3 and C4 levels are decreased** during the reaction due to massive consumption.

Q: Which of the following statements most accurately describes IgA?

IgA can be destroyed by bacterial proteases.. **Explanation** **Correct Option: B. IgA can be destroyed by bacterial proteases.** IgA is the primary immunoglobulin responsible for mucosal immunity. To counter this defense, several pathogenic bacteria (notably *Streptococcus pneumoniae*, *Haemophilus influenzae*, and *Neisseria* species) produce a specific enzyme called **IgA1 protease**. This enzyme cleaves the proline-rich hinge region of the IgA1 molecule, effectively neutralizing its ability to prevent bacterial attachment to mucosal surfaces. **Analysis of Incorrect Options:** * **Option A:** IgA **cannot** activate the classical complement pathway. It lacks the binding site for C1q. While it can activate the alternative pathway, standard complement fixation tests (which rely on the classical pathway) will be negative for IgA. * **Option C:** IgA is the **predominant** immunoglobulin in colostrum and breast milk. It provides essential passive local immunity to the neonate's gastrointestinal tract (protection against enteric pathogens). * **Option D:** IgA is the major antibody found in **all seromucous secretions**, including saliva, tears, nasal fluids, and sweat. Salivary IgA levels can indeed be used as a diagnostic marker for certain local infections or immune deficiencies. **High-Yield Clinical Pearls for NEET-PG:** * **Structure:** Secretory IgA (sIgA) exists as a **dimer** connected by a **J-chain** and contains a **Secretory Component** (which protects it from digestive enzymes). * **Selective IgA Deficiency:** The most common primary immunodeficiency; patients are often asymptomatic but may present with recurrent sinopulmonary or GI infections and are at risk for **anaphylaxis during blood transfusions** (due to anti-IgA antibodies). * **Subclasses:** IgA1 is predominant in serum; IgA2 is more prevalent in colostrum and the lower GI tract as it is more resistant to bacterial proteases.

Q: Which of the following features is common to both cytotoxic T cells and NK cells?

Effective against virus-infected cells. **Explanation:** The core similarity between **Cytotoxic T cells (CD8+ T cells)** and **Natural Killer (NK) cells** lies in their primary function: the elimination of intracellular pathogens and tumor cells. Both cell types are specialized to identify and destroy **virus-infected cells** by inducing apoptosis through the release of perforins and granzymes. * **Why Option C is correct:** Both cells act as "killers" of the immune system. While CD8+ T cells are part of the adaptive immune system (requiring MHC-I presentation), and NK cells are part of the innate immune system (acting on cells that lack MHC-I), their ultimate target—cells hijacked by viruses—is the same. **Analysis of Incorrect Options:** * **Option A:** Antibody synthesis is the exclusive function of **B-lymphocytes** (specifically plasma cells). Neither T cells nor NK cells produce antibodies. * **Option B:** While NK cells can participate in Antibody-Dependent Cellular Cytotoxicity (ADCC) via CD16, it is not a *requirement* for their primary action. CD8+ T cells do not require antibodies; they require TCR-MHC interaction. * **Option D:** Recognition of antigens with **HLA Class II** is a feature of **Helper T cells (CD4+)**. Cytotoxic T cells (CD8+) recognize antigens associated with **HLA Class I**. NK cells are actually inhibited by the presence of HLA Class I (the "missing self" hypothesis). **High-Yield Clinical Pearls for NEET-PG:** * **MHC Restriction:** CD8+ T cells are MHC-restricted (Class I), whereas NK cells are **MHC-unrestricted**. * **NK Cell Markers:** Look for **CD16** (FcγRIII) and **CD56** in questions. * **The "Missing Self":** NK cells kill cells that have down-regulated MHC-I expression—a common tactic used by viruses and tumors to evade CD8+ T cells. This makes NK cells and CD8+ cells complementary.

Q: Decreased T cell immunity is a feature of which of the following conditions?

DiGeorge syndrome. **Explanation:** **DiGeorge Syndrome (Correct Answer):** DiGeorge syndrome (22q11.2 deletion) is caused by the failure of the **3rd and 4th pharyngeal pouches** to develop. This leads to **thymic hypoplasia or aplasia**, resulting in a deficiency of mature T cells. Since the thymus is the primary site for T-cell maturation and "education," its absence leads to profound defects in cell-mediated immunity, making patients susceptible to viral, fungal, and protozoal infections. **Analysis of Incorrect Options:** * **Hyper IgM Syndrome:** This is primarily a **humoral (B-cell) immunity defect** caused by a mutation in the CD40 ligand. While it involves T-cell signaling, the hallmark is the inability of B cells to undergo class switching, leading to high IgM but low IgG, IgA, and IgE. * **Severe Congenital Neutropenia (Kostmann Syndrome):** This is a **phagocytic defect** characterized by a maturation arrest of neutrophils in the bone marrow, leading to profound neutropenia. T-cell function remains intact. * **Chronic Granulomatous Disease (CGD):** This is a **phagocytic dysfunction** caused by a defect in the NADPH oxidase enzyme. It impairs the "respiratory burst," preventing neutrophils from killing catalase-positive organisms. T-cell immunity is not primarily affected. **NEET-PG High-Yield Pearls:** * **CATCH-22 Mnemonic for DiGeorge:** **C**ardiac defects (Truncus arteriosus/TOF), **A**bnormal facies, **T**hymic hypoplasia, **C**left palate, **H**ypocalcemia (due to parathyroid hypoplasia). * **Radiology Sign:** Look for the **absence of a thymic shadow** on a newborn’s chest X-ray. * **NBT Test/DHR Flow Cytometry:** Used to diagnose CGD, not T-cell defects. * **Delayed Type Hypersensitivity (DTH):** Skin tests (like the Mantoux test) are often negative (anergy) in DiGeorge syndrome due to T-cell deficiency.

Q: What is true about interferons?

Interferons induce enzyme synthesis in the target cell.. **Explanation:** Interferons (IFNs) are low-molecular-weight proteins (cytokines) produced by host cells in response to viral infections and other stimuli. They do not act directly on viruses; instead, they function by binding to specific receptors on the surface of uninfected neighboring cells. **Why Option C is correct:** When IFNs bind to a cell, they trigger the **JAK-STAT signaling pathway**, which induces the synthesis of several antiviral enzymes. The two most important enzymes are: 1. **2',5'-oligoadenylate synthetase:** Activates RNase L, which degrades viral mRNA. 2. **Protein Kinase R (PKR):** Phosphorylates and inactivates the elongation factor eIF-2, thereby inhibiting viral protein synthesis. **Analysis of Incorrect Options:** * **Option A:** Interferons are **species-specific** (e.g., human IFN works only in human cells) but **not virus-specific**. IFN produced in response to one virus can protect against a wide range of other viruses. * **Option B:** While primarily known for antiviral activity, IFNs also have **immunomodulatory and antitumor** properties. They activate NK cells and macrophages and are used in treating conditions like Multiple Sclerosis (IFN-β) and Chronic Myeloid Leukemia. * **Option D:** Interferons are divided into **three main types** (Type I: α & β; Type II: γ; Type III: λ), not five. **High-Yield NEET-PG Pearls:** * **IFN-α:** Produced by Leucocytes; used in Hepatitis B & C and Kaposi Sarcoma. * **IFN-β:** Produced by Fibroblasts; used in Multiple Sclerosis. * **IFN-γ:** Produced by Th1 cells/NK cells; it is the primary "Macrophage Activating Factor" and is used in Chronic Granulomatous Disease (CGD).

Question 1

Which statement about IgM antibody is FALSE?

Accepted Answer

It is monomeric in nature

Answer

Has the highest molecular weight

Answer

Has the highest sedimentation coefficient

Answer

IgM is responsible for agglutination

Question 2

Which components of innate immunity are active against viral cells?

Accepted Answer

NK cells

Answer

Cytotoxic T cells

Answer

B cells

Answer

Memory B cells

Question 3

When an antigen is administered for the first time to an animal or a human being who has never been exposed to it, what is the first antibody to develop?

Accepted Answer

IgM type

Answer

IgG type

Answer

IgA type

Answer

IgE type

Question 4

Antisnake venom may cause which type of hypersensitivity reaction?

Accepted Answer

Type III hypersensitivity reactions

Answer

Type II hypersensitivity reactions

Answer

Type IV hypersensitivity reactions

Answer

Type V hypersensitivity reactions

Question 5

Which part of the IgE antibody is responsible for binding to mast cells and basophils?

Accepted Answer

Fc region

Answer

Light chain

Answer

Immunoglobulin fold

Answer

Complement binding site

Question 6

Maximum lattice formation occurs in which zone?

Accepted Answer

Zone of equivalence

Answer

Zone of antibody excess

Answer

Zone of antigen excess

Answer

Can occur in any zone

Question 7

Which of the following statements most accurately describes IgA?

Accepted Answer

IgA can be destroyed by bacterial proteases.

Answer

Complement fixation tests for IgA antibody will be positive if specific IgA antibody is present.

Answer

IgA is absent in colostrum.

Answer

IgA is not found in saliva; therefore, an IgA diagnostic test on saliva would have no value.

Question 8

Which of the following features is common to both cytotoxic T cells and NK cells?

Accepted Answer

Effective against virus-infected cells

Answer

Synthesizes antibodies

Answer

Requires antibodies to be present for action

Answer

Recognizes antigen in association with HLA class II markers

Question 9

Decreased T cell immunity is a feature of which of the following conditions?

Accepted Answer

DiGeorge syndrome

Answer

Hyper IgM syndrome

Answer

Severe congenital neutropenia

Answer

Chronic granulomatous disease

Question 10

What is true about interferons?

Accepted Answer

Interferons induce enzyme synthesis in the target cell.

Answer

Interferons are specific for individual viruses.

Answer

Interferons are protective against only viruses.

Answer

Interferons are divided into five subtypes.

Immunology — MCQs

Immunology — MCQs

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