Immunology Practice Questions

Q: The binding site for complement on the IgG molecule is located in which domain?

CH2 domain. ### Explanation The correct answer is **D. CH2 domain**. **1. Why the CH2 domain is correct:** The classical complement pathway is initiated when the **C1q** component of the C1 complex binds to the Fc portion of an antibody. For **IgG**, the specific binding site for C1q is located in the **CH2 domain** of the heavy chain. In contrast, for **IgM**, the binding site is located in the **CH3 domain**. This binding occurs only after the antibody has attached to an antigen, which induces a conformational change exposing these complement-binding sites. **2. Why the other options are incorrect:** * **A. VL domain (Variable Light):** This domain, along with the VH domain, forms the **paratope** (antigen-binding site). It is involved in recognizing and binding to specific epitopes, not complement. * **B. CL domain (Constant Light):** This domain provides structural support to the light chain and does not possess effector functions like complement fixation. * **C. CH1 domain (Constant Heavy 1):** This domain is part of the Fab fragment and acts as a spacer between the variable regions and the hinge region. It does not bind complement. **3. High-Yield Clinical Pearls for NEET-PG:** * **IgG Subclasses:** The efficiency of complement fixation follows the order: **IgG3 > IgG1 > IgG2**. Note that **IgG4** does not fix complement. * **IgM vs. IgG:** IgM is a more potent activator of complement than IgG because its pentameric structure provides multiple binding sites (CH3 domains) in close proximity. * **Fc Receptor Binding:** While CH2 binds complement, the **CH3 domain** of IgG is primarily responsible for binding to **Fc receptors** on phagocytic cells (opsonization) and mediating the long half-life of IgG via the neonatal Fc receptor (FcRn).

Q: What is the antibacterial substance present in tears that acts by splitting cell wall components?

Lysozyme. **Explanation:** The correct answer is **Lysozyme**. **1. Why Lysozyme is correct:** Lysozyme (also known as muramidase) is a key component of the innate immune system found in secretions like tears, saliva, and nasal mucus. It acts as an antibacterial agent by enzymatically cleaving the **β-1,4 glycosidic bonds** between N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM) in the **peptidoglycan** layer of bacterial cell walls. This action compromises the structural integrity of the cell wall, leading to osmotic lysis of the bacteria, particularly Gram-positive organisms. **2. Why the other options are incorrect:** * **Penicillin:** While it also targets the cell wall, it is an antibiotic drug, not a naturally occurring substance in human tears. It acts by inhibiting transpeptidase enzymes (PBP) during cell wall synthesis. * **Betalysine:** This is a heat-stable substance released by platelets during coagulation. It acts primarily against Gram-positive bacteria by disrupting the cytoplasmic membrane, not by splitting the cell wall. * **Lactoperoxidase:** Found in milk and saliva, this enzyme contributes to the non-specific immune system by generating reactive oxygen species (like hypothiocyanite) that inhibit bacterial metabolism, rather than degrading the cell wall structure. **High-Yield Facts for NEET-PG:** * **Innate Immunity:** Lysozyme is a classic example of a chemical barrier in innate immunity. * **Gram-positive vs. Gram-negative:** Lysozyme is more effective against Gram-positive bacteria because their peptidoglycan layer is exposed. Gram-negative bacteria are relatively resistant due to their protective outer membrane. * **Egg White:** Alexander Fleming discovered lysozyme; it is found in high concentrations in hen egg whites.

Q: Which of the following is NOT an antigen-presenting cell?

Microfold Cells. ### Explanation The core function of an **Antigen-Presenting Cell (APC)** is to capture antigens, process them into peptides, and present them via **MHC Class II molecules** to T-lymphocytes. **Why Microfold (M) Cells are the correct answer:** M cells are specialized epithelial cells found in the **Peyer’s patches** of the intestine. Their primary role is **transcytosis**—the transport of intact antigens from the gut lumen across the epithelial barrier to underlying lymphoid tissue. Unlike true APCs, M cells **do not process antigens** or express MHC II to activate T-cells directly. They act as "gatekeepers" rather than presenters. **Analysis of other options:** * **Follicular Dendritic Cells (FDCs):** Found in B-cell follicles of secondary lymphoid organs. They trap antigen-antibody complexes via Fc receptors and present them to B-cells. (Note: They are unique as they don't always use MHC II, but are functionally classified as APCs). * **Langerhans Cells:** These are immature dendritic cells located in the **epidermis**. They are the most potent professional APCs; once they capture an antigen, they migrate to local lymph nodes to prime naive T-cells. * **Mast Cells:** Traditionally known for Type I Hypersensitivity, recent research confirms that Mast Cells can express MHC II and costimulatory molecules, allowing them to act as unconventional APCs in certain immune responses. **High-Yield Clinical Pearls for NEET-PG:** * **Professional APCs:** Dendritic cells (most potent), Macrophages, and B-cells. * **Non-Professional APCs:** Fibroblasts, Glial cells, and Vascular Endothelial cells (can present under certain cytokine influences). * **M Cells & Pathogenesis:** Certain pathogens like *Salmonella*, *Shigella*, and Poliovirus exploit M cells as a portal of entry into the systemic circulation.

Q: Which immunoglobulin is involved in anaphylaxis?

IgE. **Explanation:** **Correct Answer: B. IgE** The correct answer is IgE because it is the primary mediator of **Type I Hypersensitivity reactions** (Anaphylaxis). When an allergen enters the body, it stimulates B-cells to produce IgE, which then binds to high-affinity receptors (**FcεRI**) on the surface of **mast cells and basophils**. Upon re-exposure, the allergen cross-links these surface-bound IgE molecules, triggering degranulation and the release of potent inflammatory mediators like histamine, leukotrienes, and prostaglandins, leading to systemic anaphylaxis. **Analysis of Incorrect Options:** * **IgA:** Primarily found in secretions (tears, saliva, colostrum, and GI mucus). It provides **mucosal immunity** and prevents the attachment of pathogens to epithelial surfaces. * **IgG:** The most abundant antibody in serum. It is involved in Type II and Type III hypersensitivity, opsonization, and toxin neutralization. It is the only antibody that **crosses the placenta**. * **IgM:** The first antibody produced in a primary immune response. It is a pentamer and is highly effective at **complement activation** and agglutination. **High-Yield Clinical Pearls for NEET-PG:** * **Prausnitz-Küstner (PK) reaction:** A classic test used to demonstrate IgE-mediated hypersensitivity. * **Heat Lability:** IgE is the most heat-labile immunoglobulin (inactivated at 56°C for 30 minutes). * **Reaginic Antibody:** IgE is also known as the reaginic antibody. * **Parasitic Infections:** IgE levels are characteristically elevated in helminthic infections (e.g., Ascariasis) as it mediates eosinophil-induced destruction of parasites.

Q: Which immunoglobulin is present on the surface of B lymphocytes and may function as an antigen receptor?

IgD. **Explanation:** The correct answer is **IgD**. **Why IgD is correct:** IgD is primarily found on the surface of **naive B lymphocytes** (B cells that have not yet encountered an antigen), where it co-expresses with IgM. Its primary physiological role is to serve as an **antigen receptor**, signaling the B cell to activate, differentiate, and initiate the humoral immune response. Unlike other antibodies, IgD is secreted into the serum in only trace amounts and has no known major effector function (like opsonization or complement activation) in its soluble form. **Why the other options are incorrect:** * **IgA:** Primarily found in secretions (tears, saliva, colostrum, GI tract) as a dimer. It provides mucosal immunity but is not a primary surface receptor for naive B cells. * **IgE:** Involved in Type I hypersensitivity (allergic) reactions and defense against helminthic parasites. It binds to high-affinity receptors on mast cells and basophils, not as a primary antigen receptor on B cells. * **IgM:** While monomeric IgM *is* also present on the surface of naive B cells as a receptor, the question specifically highlights the characteristic function of IgD. In many competitive exams, if both are listed, IgD is often the preferred answer for "surface receptor function" due to its almost exclusive role in that capacity. **High-Yield Clinical Pearls for NEET-PG:** * **B-Cell Markers:** Naive B cells express both **mIgM and mIgD**. Loss of IgD expression usually indicates B-cell activation and class switching. * **Structure:** IgD has a long hinge region, making it susceptible to proteolysis. * **Isotype Switching:** This process changes the heavy chain constant region (e.g., from IgM/IgD to IgG, IgA, or IgE) but maintains the same antigen specificity. * **Memory B cells:** Usually lack IgD.

Q: An infant is diagnosed with Bruton's agammaglobulinemia. Which of the following pathogens poses the most serious threat to this child?

Chlamydia trachomatis. **Explanation:** **Bruton’s Agammaglobulinemia (X-linked Agammaglobulinemia)** is characterized by a mutation in the **BTK gene**, leading to a failure of B-cell maturation. This results in a near-total absence of B-cells and all classes of antibodies (IgG, IgA, IgM). **Why Chlamydia trachomatis is the correct answer:** The primary defense against extracellular bacteria and certain intracellular pathogens like *Chlamydia* relies heavily on **humoral immunity (antibodies)** for opsonization and neutralization. In the absence of secretory IgA and serum IgG, patients are highly susceptible to infections of the mucous membranes. *Chlamydia trachomatis* is a significant threat because its clearance depends on an intact antibody response to prevent attachment and facilitate phagocytosis. **Why the other options are incorrect:** * **Measles, VZV, and M. tuberculosis:** These pathogens are primarily controlled by **Cell-Mediated Immunity (T-cells)**. In Bruton’s, T-cell function remains intact. Therefore, these children usually handle most viral infections (like Measles and VZV) and mycobacterial infections relatively well, as their cytotoxic T-cells and delayed-type hypersensitivity reactions are functional. **Clinical Pearls for NEET-PG:** * **Classic Presentation:** A male infant (X-linked) presenting after 6 months of age (once maternal IgG wanes) with recurrent pyogenic infections (e.g., *S. pneumoniae, H. influenzae*). * **Physical Exam Sign:** Absent or hypoplastic tonsils and adenoids (due to lack of B-cells). * **Diagnosis:** Flow cytometry showing **absent CD19/CD20+ B-cells** with normal T-cell counts. * **Contraindication:** Live viral vaccines (especially **OPV**) are contraindicated as they can cause paralytic disease in these patients.

Q: The tuberculin test:

Is dependent on memory Th1 cells. The Tuberculin Skin Test (Mantoux test) is the classic clinical example of a **Type IV (Delayed-Type) Hypersensitivity reaction**. ### Why the Correct Answer is Right The test relies on **cell-mediated immunity**. When Purified Protein Derivative (PPD) is injected intradermally, it is processed by local antigen-presenting cells (APCs). In an individual previously exposed to *M. tuberculosis*, **effector memory Th1 cells (CD4+)** recognize the antigen. These memory cells secrete cytokines (primarily **IFN-γ** and **TNF-α**), which recruit and activate macrophages, leading to local induration and erythema within 48–72 hours. ### Why Other Options are Wrong * **Option A:** The reaction is primarily mediated by **CD4+ T cells**, not CD8+ T cells. CD8+ cells are more involved in direct cytotoxicity (e.g., viral infections or graft rejection). * **Option B:** The test depends on **memory cells**, not naive cells. Naive cells would take weeks to prime a primary immune response; the 48-72 hour window is characteristic of a secondary response by pre-existing memory cells. * **Option C:** Antigen presentation is **essential**. Local macrophages and dendritic cells (Langerhans cells) must present the PPD via MHC Class II molecules to trigger the memory Th1 cells. ### High-Yield Clinical Pearls for NEET-PG * **Timing:** Maximum response occurs at **48–72 hours** (hence "delayed"). * **False Negatives (Anergy):** Can occur in miliary TB, sarcoidosis, malnutrition, Hodgkin’s lymphoma, and AIDS (due to low CD4 counts). * **False Positives:** Seen in individuals vaccinated with **BCG** or those with atypical mycobacterial infections. * **Key Cytokine:** **IFN-γ** is the most critical cytokine involved in activating macrophages to form granulomas.

Q: Which antibody is involved in Type II hypersensitivity reactions?

IgG. **Explanation:** Type II hypersensitivity is known as **Cytotoxic Hypersensitivity**. It occurs when antibodies (primarily **IgG**, and occasionally IgM) bind to antigens on the surface of specific cells or tissues. **Why IgG is correct:** In Type II reactions, the binding of **IgG** to cell-surface antigens leads to cell destruction through three main mechanisms: 1. **Complement-mediated lysis:** Activation of the classical complement pathway (MAC formation). 2. **Opsonization:** Facilitating phagocytosis by macrophages. 3. **ADCC (Antibody-Dependent Cellular Cytotoxicity):** Where NK cells destroy the target cell. **Analysis of Incorrect Options:** * **A. IgE:** Involved in **Type I (Immediate)** hypersensitivity (e.g., Anaphylaxis, Asthma). It binds to mast cells and basophils, causing degranulation. * **C. IgD:** Primarily acts as a B-cell surface receptor; it is not typically involved in any hypersensitivity reactions. * **D. IgA:** Found in mucosal secretions; it provides local immunity but is not a primary mediator of hypersensitivity. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic:** Remember the **ACID** acronym for hypersensitivity types: **A**naphylactic (I), **C**ytotoxic (II), **I**mmune-Complex (III), and **D**elayed-type (IV). * **Classic Examples of Type II:** * Autoimmune Hemolytic Anemia (AIHA) * Erythroblastosis Fetalis (Rh incompatibility) * Goodpasture Syndrome (Antibody against basement membrane) * Myasthenia Gravis and Graves' Disease (Antibody-mediated cellular dysfunction) * Rheumatic Fever (Molecular mimicry)

Q: Which of the following could prevent an allergen from reacting with a specific IgE molecule present on the mast cell membrane?

Blocking antibody. **Explanation:** The question focuses on the mechanism of preventing the **initial interaction** between an allergen and the IgE-sensitized mast cell. **1. Why "Blocking Antibody" is correct:** A blocking antibody is typically an **IgG** molecule produced during allergen immunotherapy (desensitization). These IgG antibodies have a higher affinity for the allergen than the IgE bound to mast cells. When an allergen enters the system, the IgG "intercepts" and binds to it first, effectively neutralizing the allergen before it can reach and cross-link the IgE molecules on the mast cell membrane. This prevents mast cell degranulation entirely. **2. Why other options are incorrect:** * **Antihistamines (A):** These do not prevent the allergen-IgE reaction; they act downstream by blocking H1 receptors, preventing the *effects* of histamine after it has already been released. * **Cromolyn Sodium (C):** This is a mast cell stabilizer. It prevents degranulation by inhibiting chloride channels, but it does not stop the allergen from physically reacting with the IgE on the membrane. * **Epinephrine (D):** This is a physiological antagonist. It reverses the systemic effects of anaphylaxis (via bronchodilation and vasoconstriction) but has no role in preventing the allergen-IgE binding. **Clinical Pearls for NEET-PG:** * **Immunotherapy Mechanism:** The shift from a Th2 response (IgE) to a **Th1 response (IgG4)** is the hallmark of successful desensitization. * **Type I Hypersensitivity:** Requires two separate exposures—Sensitization (IgE production) and Shocking dose (Cross-linking of IgE). * **Omalizumab:** A monoclonal antibody that binds to the Fc portion of free IgE, preventing it from binding to mast cells (another "blocking" mechanism).

Q: What is the normal ratio of CD4 to CD8 lymphocytes?

2:1. **Explanation:** The CD4:CD8 ratio is a critical biomarker of immune system health. In a healthy individual, **CD4+ T-helper cells** (which coordinate the immune response) [1] are more numerous than **CD8+ cytotoxic T-cells** (which directly kill infected or cancerous cells) [1]. The normal physiological ratio in peripheral blood is approximately **2:1**. * **Why Option B is correct:** A 2:1 ratio indicates a balanced immune system. CD4 cells typically make up about 60-70% of T-lymphocytes, while CD8 cells account for about 30%. * **Why Options A, C, and D are incorrect:** * **1:1 (Option A):** This suggests a relative depletion of CD4 cells or an expansion of CD8 cells, often seen in early stages of viral infections or chronic inflammation. * **8:1 and 10:1 (Options C & D):** These ratios are abnormally high and are not seen in healthy physiological states; they may occur in specific lymphoproliferative disorders or sarcoidosis. **Clinical Pearls for NEET-PG:** 1. **HIV/AIDS:** The hallmark of HIV progression is the selective destruction of CD4+ cells, leading to an **inverted ratio ( 3.5:1) in Bronchoalveolar Lavage (BAL) fluid.

Question 1

The binding site for complement on the IgG molecule is located in which domain?

Accepted Answer

CH2 domain

Answer

VL domain

Answer

CL domain

Answer

CH1 domain

Question 2

What is the antibacterial substance present in tears that acts by splitting cell wall components?

Accepted Answer

Lysozyme

Answer

Penicillin

Answer

Betalysine

Answer

Lactoperoxidase

Question 3

Which of the following is NOT an antigen-presenting cell?

Accepted Answer

Microfold Cells

Answer

Follicular Dendritic Cells

Answer

Mast Cells

Answer

Langerhans Cells

Question 4

Which immunoglobulin is involved in anaphylaxis?

Accepted Answer

IgE

Answer

IgA

Answer

IgG

Answer

IgM

Question 5

Which immunoglobulin is present on the surface of B lymphocytes and may function as an antigen receptor?

Accepted Answer

IgD

Answer

IgA

Answer

IgE

Answer

IgM

Question 6

An infant is diagnosed with Bruton's agammaglobulinemia. Which of the following pathogens poses the most serious threat to this child?

Accepted Answer

Chlamydia trachomatis

Answer

Measles virus

Answer

Mycobacterium tuberculosis

Answer

Varicella-zoster virus (VZV)

Question 7

The tuberculin test:

Accepted Answer

Is dependent on memory Th1 cells

Answer

Depends on activation of naive CD8 T cells by tuberculin antigen

Answer

Requires rapid activation of naive CD4 T cells

Answer

Involves no antigen presentation at the injection site

Question 8

Which antibody is involved in Type II hypersensitivity reactions?

Accepted Answer

IgG

Answer

IgE

Answer

IgD

Answer

IgA

Question 9

Which of the following could prevent an allergen from reacting with a specific IgE molecule present on the mast cell membrane?

Accepted Answer

Blocking antibody

Answer

Antihistamine

Answer

Cromolyn sodium

Answer

Epinephrine

Question 10

What is the normal ratio of CD4 to CD8 lymphocytes?

Accepted Answer

2:1

Answer

1:1

Answer

8:1

Answer

10:1

Immunology — MCQs

Immunology — MCQs

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