Immunology Practice Questions

Q: A skin test demonstrates all types of hypersensitivity except:

Type 2. ### Explanation **Why Type 2 is the Correct Answer:** Type 2 hypersensitivity (Antibody-mediated/Cytotoxic) involves antibodies (IgG or IgM) binding to antigens on the **surface of specific cells or tissues**, leading to cell lysis or dysfunction (e.g., Autoimmune Hemolytic Anemia, Myasthenia Gravis). Because this reaction occurs against fixed tissue antigens or circulating cells rather than a localized injected antigen, it **cannot be demonstrated via a routine skin test**. **Analysis of Incorrect Options:** * **Type 1 (Immediate):** Demonstrated by the **Skin Prick Test** or Intradermal Test. When an allergen is introduced, IgE bound to mast cells triggers degranulation, resulting in a "Wheal and Flare" reaction within 15–30 minutes (e.g., testing for penicillin allergy). * **Type 3 (Immune-complex):** Demonstrated by the **Arthus Reaction**. When an antigen is injected into the skin of an individual with high levels of circulating IgG, local immune complexes form in vessel walls, causing edema and necrosis within 4–8 hours. * **Type 4 (Delayed):** Demonstrated by the **Patch Test** (for Contact Dermatitis) or the **Mantoux Test** (Tuberculin test). These rely on sensitized T-cells and take 48–72 hours to show induration. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Hypersensitivity (ACID):** **A**naphlyactic (Type 1), **C**ytotoxic (Type 2), **I**mmune-Complex (Type 3), **D**elayed (Type 4). * **Type 2** is the only hypersensitivity that primarily involves the complement-mediated destruction of cells (e.g., Rh incompatibility, Goodpasture syndrome). * **Type 4** is the only type that is **cell-mediated** (T-cells) and does not involve antibodies. * The **Mantoux test** is a classic example of a Type 4 reaction used to screen for latent Tuberculosis.

Q: SCID is caused due to deficiency of?

Adenosine deaminase. **Explanation:** **Severe Combined Immunodeficiency (SCID)** is a group of rare disorders characterized by the absence of both humoral and cellular immunity. The most common autosomal recessive form of SCID is caused by a deficiency of the enzyme **Adenosine Deaminase (ADA)**. 1. **Why Adenosine Deaminase (ADA) is correct:** ADA is crucial for the purine salvage pathway. It converts adenosine to inosine and deoxyadenosine to deoxyinosine. In its absence, **deoxyadenosine** and **dATP** accumulate to toxic levels. These metabolites are particularly lethal to immature lymphocytes (T-cells and B-cells), leading to profound lymphopenia and a failure of the immune system to develop. 2. **Why the other options are incorrect:** * **Pyridoxine phosphate (Vitamin B6):** Deficiency typically leads to sideroblastic anemia, peripheral neuropathy, and seizures, but not SCID. * **Cytochrome oxidase:** Deficiency is associated with mitochondrial disorders like Leigh syndrome, affecting energy production in the brain and muscles. * **Phytanoyl CoA hydroxylase:** Deficiency of this enzyme leads to **Refsum disease**, a peroxisomal disorder characterized by the accumulation of phytanic acid, causing retinitis pigmentosa and ataxia. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** ADA deficiency is **Autosomal Recessive**, whereas the most common overall cause of SCID is **X-linked** (IL-2 receptor gamma chain mutation). * **Clinical Presentation:** Infants present with "failure to thrive," chronic diarrhea, and recurrent opportunistic infections (e.g., *Pneumocystis jirovecii*, *Candida*). * **Radiology:** A classic sign is the **absence of a thymic shadow** on a chest X-ray. * **Treatment:** ADA deficiency was the first disease treated with **Gene Therapy**. Other treatments include Bone Marrow Transplant (treatment of choice) and Enzyme Replacement Therapy (PEG-ADA).

Q: Wheal and flare reaction is what type of hypersensitivity reaction?

Type I. **Explanation:** The **Wheal and Flare reaction** is the classic clinical manifestation of **Type I (Immediate) Hypersensitivity**. **Why Type I is Correct:** Type I hypersensitivity is mediated by **IgE antibodies** bound to the surface of mast cells and basophils. Upon re-exposure to an allergen, cross-linking of these IgE molecules triggers degranulation, releasing primary mediators like **histamine**. * **The Wheal:** Histamine increases vascular permeability, leading to localized edema (soft swelling). * **The Flare:** Histamine causes vasodilation of surrounding arterioles, resulting in erythema (redness). This reaction typically occurs within minutes, which is why it is used in "Skin Prick Tests" to identify allergens. **Why Other Options are Incorrect:** * **Type II (Antibody-mediated):** Involves IgG or IgM attacking antigens on specific cell surfaces or tissues (e.g., Erythroblastosis fetalis, Myasthenia gravis). It does not produce an immediate wheal. * **Type III (Immune-complex mediated):** Caused by the deposition of antigen-antibody complexes in tissues, leading to complement activation (e.g., Arthus reaction, SLE). The Arthus reaction is inflammatory but occurs over 4–10 hours, not minutes. * **Type IV (Delayed-type):** Mediated by T-cells rather than antibodies. The reaction (e.g., Mantoux test) takes 48–72 hours to develop and is characterized by induration rather than a soft wheal. **High-Yield Clinical Pearls for NEET-PG:** * **Coombs and Gell Classification:** Type I (Anaphylactic), Type II (Cytotoxic), Type III (Immune-complex), Type IV (Delayed). * **Key Cells:** Mast cells are the central effector cells in Type I reactions. * **Common Examples of Type I:** Anaphylaxis, Urticaria, Atopic dermatitis, and Allergic rhinitis. * **The Arthus Reaction (Type III)** is often confused with the Wheal and Flare; remember that Arthus is delayed (hours) and involves localized vasculitis.

Q: The prototype of type-II hypersensitivity reaction is:

Autoimmune hemolytic anemia. ### Explanation **Type II Hypersensitivity** (Cytotoxic Hypersensitivity) is mediated by **IgG or IgM** antibodies directed against antigens present on the surface of specific cells or tissues. This leads to cell destruction via the complement system, opsonization (phagocytosis), or antibody-dependent cellular cytotoxicity (ADCC). **Why Autoimmune Hemolytic Anemia (AIHA) is correct:** In AIHA, antibodies (usually IgG) are produced against self-antigens on the **Red Blood Cell (RBC) membrane**. These coated RBCs are then destroyed by splenic macrophages or complement-mediated lysis. This is a classic example of tissue-specific damage, the hallmark of Type II reactions. **Analysis of Incorrect Options:** * **Arthus Reaction (Option A):** This is a localized **Type III** hypersensitivity reaction. It involves the formation of immune complexes (antigen-antibody) that deposit in vessel walls, leading to vasculitis and necrosis. * **Systemic Lupus Erythematosus (Option B):** SLE is the prototype for **Type III** hypersensitivity. It involves circulating immune complexes that deposit in various organs (kidneys, joints, skin), causing systemic inflammation. * **Contact Dermatitis (Option D):** This is a **Type IV** (Delayed-type) hypersensitivity reaction. It is mediated by T-cells (CD4+ and CD8+) rather than antibodies, typically occurring 48–72 hours after exposure to allergens like nickel or poison ivy. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Hypersensitivity:** **ACID** (Type I: **A**naphylactic/Allergic; Type II: **C**ytotoxic; Type III: **I**mmune Complex; Type IV: **D**elayed). * **Other Type II Examples:** Goodpasture syndrome, Myasthenia Gravis, Graves' disease, and Rheumatic fever. * **Coombs Test:** The Direct Antiglobulin Test (Coombs test) is the gold standard for diagnosing Type II reactions involving RBCs (like AIHA and Erythroblastosis Fetalis).

Q: The Casoni test is associated with which type of hypersensitivity reaction?

Type I Hypersensitivity reactions. **Explanation:** The **Casoni test** is an immediate hypersensitivity skin test used for the diagnosis of **Hydatid disease** (caused by *Echinococcus granulosus*). **Why Type I is correct:** When a small amount of sterile hydatid fluid is injected intradermally, it reacts with specific **IgE antibodies** bound to the surface of mast cells in a sensitized individual. This triggers degranulation and the release of histamine, resulting in a **"wheal and flare"** reaction within 15–20 minutes. This immediate, IgE-mediated response is the hallmark of a **Type I Hypersensitivity reaction**. **Why other options are incorrect:** * **Type II (Cytotoxic):** Involves IgG/IgM antibodies binding to cell surface antigens (e.g., Rh incompatibility). Casoni test involves free antigen-antibody interaction on mast cells, not cell lysis. * **Type III (Immune-complex):** Involves deposition of antigen-antibody complexes in tissues (e.g., SLE). While a late-phase reaction (8 hours) can occur in the Casoni test, the diagnostic component is the immediate Type I response. * **Type IV (Delayed-type):** Mediated by T-cells (e.g., Mantoux test). These take 48–72 hours to manifest, whereas the Casoni test is read almost immediately. **High-Yield Clinical Pearls for NEET-PG:** * **Antigen used:** Sterile fluid from human or sheep hydatid cysts. * **Sensitivity/Specificity:** The test is highly sensitive but has **low specificity** due to cross-reactivity with *Taenia* and other helminths. * **Current Status:** It is largely obsolete and has been replaced by more specific serological tests (ELISA, Immunoblot) and imaging (USG/CT). * **Other Type I Skin Tests:** Schick test (Diphtheria - though primarily a toxin-antitoxin test, it has an allergic component) and various allergen prick tests.

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

Bipolar cell. **Explanation:** Antigen-presenting cells (APCs) are specialized cells that capture antigens, process them into peptides, and present them via Major Histocompatibility Complex (MHC) molecules to T-cells. **Why Bipolar cell is the correct answer:** Bipolar cells are **interneurons** found in the retina of the eye. Their primary function is the transmission of visual signals from photoreceptors (rods and cones) to ganglion cells. They lack MHC-II expression and do not participate in the immune response or antigen processing. **Analysis of other options:** * **Dendritic cells:** These are the most potent **Professional APCs**. They are the only cells capable of activating naive T-cells, bridging innate and adaptive immunity. * **Follicular dendritic cells (FDCs):** Located in the germinal centers of B-cell follicles, they trap antigens (as immune complexes) and present them to B-cells. Note: Unlike regular dendritic cells, FDCs are not bone marrow-derived. * **Tissue macrophages:** These are professional APCs (part of the Mononuclear Phagocyte System) that phagocytose pathogens and present antigens to CD4+ T-helper cells via MHC-II. **High-Yield Clinical Pearls for NEET-PG:** * **Professional APCs:** Dendritic cells (most potent), Macrophages, and B-lymphocytes. All express **MHC-II**. * **Non-professional APCs:** Endothelial cells and fibroblasts (can be induced by IFN-γ). * **MHC Restriction:** APCs present exogenous antigens via **MHC-II to CD4+ T-cells**, while endogenous antigens are presented via **MHC-I to CD8+ T-cells**. * **Langerhans cells:** These are specialized dendritic cells found in the stratum spinosum of the skin.

Q: Cellular immunity is induced by?

TH1 cells. **Explanation:** Cellular immunity (Cell-Mediated Immunity or CMI) is primarily mediated by T-lymphocytes. The correct answer is **TH1 cells** because they are the primary orchestrators of the CMI response. 1. **Why TH1 cells are correct:** Upon activation by IL-12, naive T-helper cells differentiate into **TH1 cells**. These cells secrete **Interferon-gamma (IFN-γ)** and **IL-2**, which activate macrophages and cytotoxic T-cells (CD8+). This pathway is essential for eliminating intracellular pathogens (like *M. tuberculosis*) and delayed-type hypersensitivity (DTH) reactions. 2. **Why other options are incorrect:** * **TH2 cells:** These are responsible for **Humoral Immunity**. They secrete IL-4, IL-5, and IL-13, which promote B-cell activation, class switching to IgE, and eosinophil recruitment. * **NK-cells:** While they are part of the innate cellular response, they do not "induce" the adaptive cellular immune memory; they act as the first line of defense against virally infected or tumor cells. * **Dendritic cells:** These are **Antigen-Presenting Cells (APCs)**. They initiate the immune response by presenting antigens to T-cells, but they are the "triggers" rather than the mediators of the specialized cellular immune arm. **High-Yield Clinical Pearls for NEET-PG:** * **TH1 Cytokines:** IFN-γ, IL-2, TNF-β (Lead to CMI). * **TH2 Cytokines:** IL-4, IL-5, IL-6, IL-10, IL-13 (Lead to Humoral Immunity). * **Leprosy Link:** Tuberculoid leprosy is associated with a strong **TH1 response** (contained infection), whereas Lepromatous leprosy is associated with a **TH2 response** (disseminated infection). * **Mnemonic:** **1** looks like an **I** (Intracellular/IFN-γ); **2** is for **B** (B-cells/Humoral).

Q: What is the function of IL-4?

Inhibiting IL-1. **Explanation:** Interleukin-4 (IL-4) is a key cytokine produced primarily by **Th2 cells**, mast cells, and basophils. Its primary role is to drive the humoral immune response. **Why Option A is Correct:** IL-4 acts as an **anti-inflammatory cytokine**. It downregulates the production of pro-inflammatory cytokines like **IL-1**, TNF-alpha, and IL-6. Specifically, IL-4 induces the production of the **IL-1 receptor antagonist (IL-1Ra)**, which competitively inhibits IL-1 activity, thereby limiting the inflammatory damage. **Analysis of Incorrect Options:** * **B. Chemotaxis:** This is primarily the function of **IL-8** (the major neutrophil chemoattractant) and C5a. * **C. Vasodilation:** This is mediated by chemical mediators like **Histamine**, Prostaglandins (PGE2), and Nitric Oxide (NO), rather than IL-4. * **D. Inhibiting Macrophages:** While IL-4 does antagonize the "classical activation" (M1) of macrophages, the most potent inhibitor of macrophage function is **IL-10** and **TGF-beta**. IL-4 actually promotes "alternative activation" (M2) of macrophages, which is involved in tissue repair. **High-Yield Clinical Pearls for NEET-PG:** * **Class Switching:** IL-4 is the primary driver for B-cell class switching to **IgE** and **IgG4**. (Mnemonic: *4-E-G*). * **Th2 Differentiation:** IL-4 promotes the differentiation of naive T-cells (Th0) into Th2 cells while inhibiting Th1 differentiation. * **Atopy:** Overproduction of IL-4 is associated with Type I Hypersensitivity reactions (asthma, eczema, and anaphylaxis). * **Major Anti-inflammatory Cytokines:** Remember **IL-4, IL-10, and TGF-beta**.

Q: Who received the Nobel Prize for the discovery of split genes?

Susumu Tonegawa. **Explanation:** The correct answer is **Susumu Tonegawa**. In 1987, he was awarded the Nobel Prize in Physiology or Medicine for his discovery of the genetic mechanism that generates **antibody diversity**. **Why Susumu Tonegawa is correct:** The human body can produce billions of different antibodies despite having a limited number of genes. Tonegawa demonstrated that immunoglobulin genes are not continuous but exist as **"split genes"** (segments). He showed that B cells undergo **somatic recombination**, where different gene segments (V, D, and J) are shuffled and rearranged. This "mix-and-match" process, followed by RNA splicing, allows a small amount of DNA to code for a vast array of antigen-binding sites. **Analysis of Incorrect Options:** * **Burnet (Sir Frank Macfarlane Burnet):** Best known for the **Clonal Selection Theory** and the discovery of acquired immunological tolerance (Nobel Prize 1960). * **Niels K. Jerne:** Awarded the Nobel Prize (1984) for theories regarding the specificity in development and control of the immune system (e.g., the **Immune Network Theory**). * **Paul Ehrlich:** Known as the father of chemotherapy and for his **"Side-Chain Theory"** of antibody formation (Nobel Prize 1908). **High-Yield Clinical Pearls for NEET-PG:** * **V(D)J Recombination:** Occurs in the primary lymphoid organs (Bone marrow for B cells). * **RAG-1 and RAG-2:** These are the recombinase enzymes essential for this process. Deficiency leads to **Omenn Syndrome** or **SCID**. * **Antibody Diversity Mechanisms:** 1. Multiple germline segments, 2. Combinatorial VDJ joining, 3. Junctional diversity (TdT enzyme), 4. Somatic hypermutation.

Question 1

A skin test demonstrates all types of hypersensitivity except:

Accepted Answer

Type 2

Answer

Type 1

Answer

Type 3

Answer

Type 4

Question 2

SCID is caused due to deficiency of?

Accepted Answer

Adenosine deaminase

Answer

Pyridoxine phosphate

Answer

Cytochrome oxidase

Answer

Phyntanoyl CoA

Question 3

Wheal and flare reaction is what type of hypersensitivity reaction?

Accepted Answer

Type I

Answer

Type II

Answer

Type III

Answer

Type IV

Question 4

The prototype of type-II hypersensitivity reaction is:

Accepted Answer

Autoimmune hemolytic anemia

Answer

Arthus reaction

Answer

Systemic Lupus Erythematosus (SLE)

Answer

Contact dermatitis

Question 5

Which cells are primarily concerned with cell-mediated immunity?

Accepted Answer

T-Lymphocytes

Answer

B-Lymphocytes

Answer

Eosinophils

Answer

Monocytes

Question 6

The Casoni test is associated with which type of hypersensitivity reaction?

Accepted Answer

Type I Hypersensitivity reactions

Answer

Type II Hypersensitivity reactions

Answer

Type III Hypersensitivity reactions

Answer

Type IV Hypersensitivity reactions

Question 7

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

Accepted Answer

Bipolar cell

Answer

Dendritic cell

Answer

Follicular dendritic cell

Answer

Tissue macrophage

Question 8

Cellular immunity is induced by?

Accepted Answer

TH1 cells

Answer

NK-cells

Answer

Dendritic cells

Answer

TH2 cells

Question 9

What is the function of IL-4?

Accepted Answer

Inhibiting IL-1

Answer

Chemotaxis

Answer

Vasodilation

Answer

Inhibiting macrophages

Question 10

Who received the Nobel Prize for the discovery of split genes?

Accepted Answer

Susumu Tonegawa

Answer

Burnet

Answer

Neils K Jerne

Answer

Paul Ehrlich

Immunology — MCQs

Immunology — MCQs

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