Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 521: CD4 count refers to which type of cell?

A. T helper cells (Correct Answer)
B. B cells
C. Cytotoxic cells
D. Both B and T cells

Explanation: **Explanation:** **CD4+ cells**, also known as **T helper cells**, are a subtype of T lymphocytes that play a central role in orchestrating the immune response. They recognize antigens presented by **MHC Class II** molecules on professional antigen-presenting cells (APCs). Once activated, they secrete cytokines that help activate B cells (for antibody production) and Cytotoxic T cells (for cell-mediated immunity). **Analysis of Options:** * **Option A (Correct):** CD4 is the characteristic surface marker for T helper cells. * **Option B (Incorrect):** B cells are characterized by markers such as **CD19, CD20, and CD21**. They do not express CD4. * **Option C (Incorrect):** Cytotoxic T cells are characterized by the **CD8** surface marker and interact with MHC Class I molecules. * **Option D (Incorrect):** CD4 is specific to the helper subset of T cells and is not found on B cells. **High-Yield Clinical Pearls for NEET-PG:** * **HIV Pathogenesis:** The HIV virus selectively infects and destroys CD4+ T cells by binding to the CD4 molecule via its **gp120** envelope protein. * **AIDS Definition:** In HIV-infected individuals, a CD4 count **<200 cells/mm³** (or a percentage <14%) is the diagnostic threshold for AIDS. * **MHC Restriction Rule:** Remember the **"Rule of 8"**: * CD4 × MHC II = 8 * CD8 × MHC I = 8 * **Normal CD4/CD8 Ratio:** In a healthy individual, the ratio is approximately **2:1**. This ratio is typically inverted (<1) in patients with AIDS.

Question 522: Interferon is what type of molecule?

A. Protein (Correct Answer)
B. Lipid
C. Polysaccharide
D. Nucleic acid

Explanation: **Explanation:** Interferons (IFNs) are a group of signaling proteins, specifically **cytokines**, released by host cells in response to the presence of several viruses. They are chemically classified as **glycoproteins** (proteins with a carbohydrate side chain). Their primary function is to "interfere" with viral replication by triggering the protective defenses of the immune system that eradicate pathogens. * **Why Protein is Correct:** Interferons are encoded by specific genes and synthesized via the ribosomal pathway. They function by binding to specific cell-surface receptors, initiating a signaling cascade (JAK-STAT pathway) that leads to the synthesis of antiviral proteins. * **Why other options are incorrect:** * **Lipids:** These are hydrophobic molecules used for membranes or energy storage; they do not possess the complex structural specificity required for cytokine signaling. * **Polysaccharides:** These are complex carbohydrates (like bacterial capsules). While IFNs have a carbohydrate component, their functional backbone is polypeptide-based. * **Nucleic acids:** These (DNA/RNA) carry genetic information. While nucleic acids often *trigger* interferon production, they do not constitute the molecule itself. **High-Yield Clinical Pearls for NEET-PG:** * **Classification:** * **Type I:** IFN-α (Leukocytes) and IFN-β (Fibroblasts). Primarily antiviral. * **Type II:** IFN-γ (T-cells and NK cells). Primarily immunomodulatory (activates macrophages). * **Mechanism:** They do not kill viruses directly; they induce an "antiviral state" in neighboring uninfected cells. * **Clinical Use:** IFN-α is used in the treatment of Hepatitis B, Hepatitis C, Kaposi sarcoma, and Hairy cell leukemia.

Question 523: Which category of immune disorders best describes Chediak-Higashi syndrome?

A. Disorders of specific immunity
B. Disorders of complement
C. Disorders of phagocytosis (Correct Answer)
D. Secondary immunodeficiencies

Explanation: **Explanation:** **Chediak-Higashi Syndrome (CHS)** is a rare autosomal recessive disorder caused by a mutation in the **LYST gene** (Lysosomal Trafficking Regulator). This defect leads to impaired microtubule assembly, which prevents the fusion of phagosomes with lysosomes. Consequently, phagocytes (neutrophils and macrophages) can ingest bacteria but cannot kill them effectively because the **phagolysosome** fails to form. This places CHS firmly in the category of **Disorders of Phagocytosis**. **Analysis of Options:** * **Option A (Specific Immunity):** These involve defects in B-cells (antibody production) or T-cells (cell-mediated immunity), such as SCID or X-linked Agammaglobulinemia. CHS primarily affects the innate cellular response. * **Option B (Complement):** These involve deficiencies in proteins like C3 (recurrent infections) or C5-C9 (Neisserial infections). CHS is a cellular defect, not a humoral protein deficiency. * **Option D (Secondary Immunodeficiencies):** These are acquired due to external factors like HIV, malnutrition, or chemotherapy. CHS is a primary (congenital/genetic) immunodeficiency. **Clinical Pearls for NEET-PG:** 1. **Pathognomonic Finding:** Presence of **giant intracytoplasmic granules** in neutrophils and platelets on a peripheral blood smear. 2. **Clinical Triad:** * **Partial Oculocutaneous Albinism** (melanocyte transport defect). * **Recurrent Pyogenic Infections** (Staph and Strep). * **Neurological abnormalities** (peripheral neuropathy). 3. **Bleeding Diathesis:** Due to defective dense granules in platelets. 4. **Accelerated Phase:** A life-threatening lymphohistiocytic infiltration of organs (HLH-like syndrome).

Question 524: Which is the pentameric antibody?

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

Explanation: ### Explanation **Correct Answer: C. IgM** **Why IgM is the correct answer:** Immunoglobulin M (IgM) is the largest antibody in the human body. In its secreted form, it exists as a **pentamer** (five basic Y-shaped units) held together by disulfide bonds and a specialized polypeptide called the **J-chain** (Joining chain). Due to its pentameric structure, it has 10 antigen-binding sites, giving it the highest **avidity** among all immunoglobulins. It is the first antibody to appear in response to an initial exposure to an antigen. **Analysis of Incorrect Options:** * **IgD (Option A):** Exists exclusively as a **monomer**. It is primarily found on the surface of B-cells, serving as an antigen receptor. * **IgG (Option B):** Exists as a **monomer**. It is the most abundant antibody in serum and the only one capable of crossing the placenta. * **IgA (Option C):** Exists as a **monomer** in serum but as a **dimer** (two units) in secretions (like saliva, tears, and breast milk). It also contains a J-chain in its dimeric form. **NEET-PG High-Yield Pearls:** * **Valency:** IgM has a theoretical valency of 10, but due to steric hindrance, it usually binds to 5 antigens simultaneously. * **Evolutionary Fact:** IgM is the oldest immunoglobulin class phylogenetically. * **Clinical Marker:** Presence of IgM in a patient’s serum indicates a **recent/acute infection**, whereas IgG indicates a past infection or chronic state. * **Size:** Because of its large size (molecular weight ~900,000 Da), IgM is confined to the intravascular compartment and cannot cross the placenta. * **Complement Activation:** IgM is the most efficient activator of the **classical complement pathway**.

Question 525: How many subclasses does IgG have?

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

Explanation: **Explanation:** Immunoglobulin G (IgG) is the most abundant class of antibody in human serum, accounting for approximately 75–80% of total serum immunoglobulins. It is divided into **four subclasses** based on structural differences in the constant region of the heavy chains ($\gamma$ chains), specifically in the hinge region and the number of disulfide bonds. * **Why Option D is Correct:** IgG consists of four distinct subclasses: **IgG1, IgG2, IgG3, and IgG4**. These subclasses are numbered in order of their decreasing concentration in the serum (IgG1 > IgG2 > IgG3 > IgG4). They differ in their biological properties, such as their ability to cross the placenta and activate the classical complement pathway. * **Why Options A, B, and C are Incorrect:** These options do not reflect the established classification of IgG. While other immunoglobulins have fewer subclasses (e.g., IgA has two: IgA1 and IgA2), IgG is uniquely characterized by four. **High-Yield Facts for NEET-PG:** * **Placental Transfer:** All four subclasses cross the placenta, but **IgG2** crosses with the least efficiency. This provides passive immunity to the fetus. * **Complement Activation:** **IgG3** is the most potent activator of the classical complement pathway, followed by IgG1 and IgG2. **IgG4 does not activate complement.** * **Half-life:** The average half-life of IgG is **23 days** (the longest among all Igs), except for IgG3, which has a shorter half-life of about 7 days. * **Clinical Correlation:** IgG4-related disease (IgG4-RD) is a fibro-inflammatory condition characterized by elevated serum IgG4 levels and tissue infiltration by IgG4-positive plasma cells.

Question 526: All of the following are immune complex diseases except?

A. Serum sickness
B. Farmer's lung
C. Systemic lupus erythematosus
D. Graft rejection (Correct Answer)

Explanation: **Explanation:** The question tests the classification of hypersensitivity reactions. The correct answer is **Graft rejection** because it is primarily a **Type IV (Cell-mediated) hypersensitivity reaction**, whereas the other options are examples of **Type III (Immune complex-mediated) hypersensitivity**. **1. Why Graft Rejection is the Correct Answer:** Acute graft rejection is mediated by T-lymphocytes (CD8+ cytotoxic T cells and CD4+ helper T cells) reacting against donor MHC antigens. While hyperacute rejection involves pre-formed antibodies (Type II), the classic process of rejection is the hallmark of Type IV hypersensitivity, not the deposition of circulating immune complexes. **2. Analysis of Incorrect Options (Type III Hypersensitivity):** * **Serum Sickness:** A systemic Type III reaction occurring when foreign serum proteins are injected. Antigen-antibody complexes form in the blood and deposit in tissues (joints, kidneys), causing fever, rash, and arthritis. * **Farmer’s Lung:** A form of Hypersensitivity Pneumonitis. It occurs when inhaled fungal spores (e.g., *Saccharopolyspora rectivirgula*) react with specific IgG antibodies, forming local immune complexes in the alveoli. * **Systemic Lupus Erythematosus (SLE):** The prototype of systemic Type III hypersensitivity. Auto-antibodies bind to self-antigens (like DNA), forming complexes that deposit in small vessels, leading to glomerulonephritis and vasculitis. **High-Yield Clinical Pearls for NEET-PG:** * **Type III mnemonic:** "Immune Complex" (Ag-Ab complexes + Complement activation). * **Arthus Reaction:** A localized Type III reaction (e.g., swelling after a booster vaccine). * **Key Triad of Serum Sickness:** Fever, Urticaria, and Arthralgia. * **Graft vs. Host Disease (GVHD):** Occurs when donor T-cells attack the recipient's tissues; also a Type IV reaction.

Question 527: Which of the following conditions is characterized by normal or slightly reduced IgG levels?

A. Wiskott-Aldrich syndrome (Correct Answer)
B. Selective IgA deficiency
C. DiGeorge syndrome
D. Common variable immunodeficiency

Explanation: **Explanation:** **Wiskott-Aldrich Syndrome (WAS)** is an X-linked recessive disorder caused by a mutation in the *WASP* gene, leading to defective actin polymerization in hematopoietic cells. The characteristic immunoglobulin profile in WAS is unique: **IgM levels are low**, while **IgA and IgE levels are elevated**. Crucially, **IgG levels are typically normal or only slightly reduced**, making it the correct answer. **Analysis of Incorrect Options:** * **Selective IgA Deficiency:** This is the most common primary immunodeficiency. It is characterized by a profound deficiency of IgA (<7 mg/dL) with **normal levels of IgG and IgM**. * **DiGeorge Syndrome:** This is a T-cell deficiency caused by the failure of the 3rd and 4th pharyngeal pouches to develop (22q11 deletion). While B-cell numbers are normal, antibody production (including IgG) may be impaired due to a lack of T-cell help, but the primary defect is cellular, not a specific "normal to slightly reduced" IgG pattern. * **Common Variable Immunodeficiency (CVID):** This condition is characterized by a **significant decrease in IgG**, along with low IgA and/or IgM. The hallmark of CVID is the failure of B-cells to differentiate into plasma cells. **High-Yield Clinical Pearls for NEET-PG:** * **WAS Triad:** Thrombocytopenia (with small platelets), Eczema, and Recurrent infections (primarily encapsulated organisms). * **Mnemonic for WAS:** **TIE** (Thrombocytopenia, Infections, Eczema). * **Laboratory Marker:** Low IgM + High IgA/IgE + Normal/Low IgG. * **Complications:** Increased risk of autoimmune diseases and B-cell lymphomas.

Question 528: Which cytokine is secreted by TH2 cells?

A. IL-2
B. IFN-g
C. IL-5 (Correct Answer)
D. TNF-a

Explanation: ### Explanation The differentiation of **CD4+ T-helper (Th) cells** into specific subsets (Th1, Th2, Th17) is a high-yield concept in immunology. This differentiation depends on the cytokine environment and results in the secretion of specific effector cytokines. **Why IL-5 is Correct:** **Th2 cells** are primarily involved in the humoral immune response, defense against helminthic parasites, and allergic reactions. They characteristically secrete **IL-4, IL-5, IL-10, and IL-13**. * **IL-5** specifically acts as an eosinophil chemoattractant and activator, promoting their growth and differentiation, which is essential for killing parasites. **Analysis of Incorrect Options:** * **A. IL-2:** Primarily secreted by **Th1 cells**. It acts as a T-cell growth factor, promoting the proliferation of T-cells (autocrine/paracrine) and NK cells. * **B. IFN-γ (Interferon-gamma):** The signature cytokine of **Th1 cells**. It activates macrophages and promotes B-cell class switching to IgG, facilitating the cell-mediated immune response against intracellular pathogens. * **D. TNF-α:** A pro-inflammatory cytokine produced mainly by **macrophages** and **Th1 cells**. It is involved in systemic inflammation and the formation of granulomas. **High-Yield NEET-PG Pearls:** 1. **Th1 vs. Th2 Balance:** Th1 is for **intracellular** pathogens (Type 1 response); Th2 is for **extracellular** pathogens/parasites (Type 2 response). 2. **Cross-Inhibition:** IFN-γ (from Th1) inhibits Th2 proliferation, while IL-10 (from Th2) inhibits Th1 cytokine production. 3. **Key Transcription Factors:** **T-bet** for Th1; **GATA-3** for Th2. 4. **Clinical Correlation:** Atopic diseases (asthma, eczema) are driven by an overactive Th2 response leading to high IgE and eosinophilia.

Question 529: Which one of the following hypotheses may be sufficient to explain non-precipitation in an antigen-antibody system?

A. The antigen has a multivalent determinant
B. The antigen has a single, non-repeated determinant
C. The antibody has been cleaved to divalent Fab' fragments (Correct Answer)
D. The antibody has been cleaved to divalent Fab'2 fragments

Explanation: ### Explanation **1. Why Option C is Correct (The Underlying Concept)** Precipitation occurs when a **multivalent antigen** reacts with a **multivalent antibody** (usually bivalent IgG) to form a large, insoluble cross-linked lattice. For this lattice to form, the antibody must be able to bridge two different antigen molecules. When an antibody is cleaved into **Fab fragments** (using the enzyme papain), the resulting fragments are **monovalent**. While they can still bind to the antigen's epitope, they cannot bridge two antigens together. This prevents the formation of a lattice, resulting in a lack of precipitation. Note: The question uses the term "divalent Fab' fragments" which is a common nomenclature error in some texts; however, in the context of competitive exams, it refers to the monovalent binding capacity of individual Fab units that prevents cross-linking. **2. Why the Other Options are Incorrect** * **Option A:** A multivalent determinant on an antigen actually *promotes* lattice formation and precipitation. * **Option B:** While a single determinant might limit lattice size, if the determinant is repeated (polyvalent), precipitation can still occur. However, monovalent Fab fragments are a more definitive cause for the total failure of precipitation. * **Option D:** **F(ab')2 fragments** (produced by pepsin) are **divalent**. Because they have two binding sites, they *can* cross-link antigens and *will* cause precipitation, unlike the monovalent Fab fragments. **3. NEET-PG High-Yield Pearls** * **Papain Digestion:** Cleaves IgG at the hinge region into **two monovalent Fab** fragments and one Fc fragment. (No precipitation). * **Pepsin Digestion:** Cleaves IgG below the hinge region into **one divalent F(ab')2** fragment and degraded Fc sub-fragments. (Precipitation occurs). * **Prozone Phenomenon:** Lack of precipitation due to **antibody excess**. * **Postzone Phenomenon:** Lack of precipitation due to **antigen excess**. * **Zone of Equivalence:** The specific ratio where optimal lattice formation and maximal precipitation occur.

Question 530: An immunologist sees a child with a suspected primary immunodeficiency and orders a nitroblue tetrazolium test. What condition is she screening the child for?

A. Chediak-Higashi syndrome
B. Tuftsin deficiency
C. Chronic granulomatous disease (Correct Answer)
D. Wiskott-Aldrich syndrome

Explanation: ### Explanation **Correct Answer: C. Chronic granulomatous disease (CGD)** **Mechanism:** Chronic Granulomatous Disease is caused by a genetic defect in the **NADPH oxidase enzyme complex**. This enzyme is responsible for the "respiratory burst," which produces reactive oxygen species (like superoxide radicals) necessary for killing phagocytosed microorganisms. The **Nitroblue Tetrazolium (NBT) test** is a functional assay for this process. * **Normal cells:** NADPH oxidase reduces the yellow NBT dye into deep blue/purple **formazan crystals**. * **CGD cells:** Due to the enzyme deficiency, they cannot reduce the dye, and the cells remain **colorless/yellow** (NBT negative). **Why other options are incorrect:** * **A. Chediak-Higashi syndrome:** This is a defect in **lysosomal trafficking (LYST gene)**, leading to giant granules and impaired chemotaxis, not a defect in the respiratory burst. * **B. Tuftsin deficiency:** Tuftsin is a tetrapeptide that enhances phagocytosis; its deficiency leads to increased infections but does not affect the NADPH oxidase pathway. * **D. Wiskott-Aldrich syndrome:** This is a triad of **thrombocytopenia (small platelets), eczema, and immunodeficiency** caused by a defect in actin cytoskeleton reorganization (WASP gene). **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most commonly **X-linked recessive** (CYBB gene mutation). * **Microbiology:** Patients are highly susceptible to **Catalase-positive organisms** (e.g., *Staphylococcus aureus, Aspergillus, Nocardia, Serratia marcescens*) because these organisms neutralize their own H₂O₂. * **Modern Diagnosis:** While NBT was the traditional gold standard, the **Dihydrorhodamine (DHR) flow cytometry test** is now the preferred diagnostic tool due to higher sensitivity. * **Pathology:** Characterized by the formation of **granulomas** in various organs as the body tries to wall off persistent intracellular infections.

Practice by Chapter

Cells and Organs of Immune System

Practice Questions

Innate Immunity

Practice Questions

Adaptive Immunity

Practice Questions

Antigens and Antibodies

Practice Questions

Major Histocompatibility Complex

Practice Questions

Complement System

Practice Questions

Cytokines and Chemokines

Practice Questions

Hypersensitivity Reactions

Practice Questions

Autoimmunity and Autoimmune Diseases

Practice Questions

Immunodeficiency Disorders

Practice Questions

Transplantation Immunology

Practice Questions

Tumor Immunology

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Immunology — MCQs

Immunology — MCQs

On this page

Practice by Chapter

Want unlimited practice?