Immunology — MCQs
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A young patient presents with severe recurrent pyogenic bacterial infections, yet has normal T-cell and B-cell numbers. Testing reveals a defect in the CD40 ligand of the patient's CD4 T-helper cells. Which immunoglobulin, characterized by its presence as a monomer on B-cell surfaces, a pentamer in serum, and its initial appearance in the primary immune response, is significantly elevated in this patient?
Which of the following statements regarding IgE antibodies is NOT true?
Which of the following statements is FALSE regarding acquired immunity?
Mast cells synthesize and/or secrete which of the following substances?
The technique of immunoblotting used to analyze RNA is named as?
A 21-year-old woman has a history since childhood of recurrent episodes of swelling of the submucosal and subcutaneous tissue of the gastrointestinal and respiratory tracts. Her C1 inhibitor level is less than 5% of the reference value. These findings support a diagnosis of:
What is the most important cytokine for type II lepra reaction?
What region of the immunoglobulin molecule contains the antigen binding site?
What is the heterophile agglutination test?
Which of the following is coded by the HLA III gene?
Immunology Indian Medical PG Practice Questions and MCQs
Question 541: A young patient presents with severe recurrent pyogenic bacterial infections, yet has normal T-cell and B-cell numbers. Testing reveals a defect in the CD40 ligand of the patient's CD4 T-helper cells. Which immunoglobulin, characterized by its presence as a monomer on B-cell surfaces, a pentamer in serum, and its initial appearance in the primary immune response, is significantly elevated in this patient?
- A. IgG
- B. IgA
- C. IgM (Correct Answer)
- D. IgD
Explanation: **Explanation:** The clinical presentation describes **Hyper-IgM Syndrome (Type 1)**, an X-linked immunodeficiency. The core defect lies in the **CD40 ligand (CD154)** on T-cells, which fails to interact with the **CD40 receptor** on B-cells. This interaction is mandatory for **Isotype Class Switching** and **Somatic Hypermutation**. 1. **Why IgM is correct:** Because B-cells cannot receive the "signal" to switch from producing IgM to other classes (IgG, IgA, or IgE), they continue to produce only IgM. Consequently, serum levels of IgM are normal to significantly elevated, while other isotopes are severely deficient. IgM is the first antibody produced in a primary response, exists as a **monomer** on B-cell surfaces (BCR), and forms a **pentamer** (with a J-chain) in serum. 2. **Why other options are incorrect:** * **IgG:** Levels are low because class switching from IgM to IgG is blocked. IgG is the most abundant serum Ig and crosses the placenta. * **IgA:** Levels are low due to the class-switch defect. IgA is primarily found in secretions (dimer) and protects mucosal surfaces. * **IgD:** While present on B-cell surfaces alongside IgM, it is not the primary antibody elevated in this syndrome and does not exist as a pentamer in serum. **High-Yield Clinical Pearls for NEET-PG:** * **Genetics:** Most common form is X-linked (CD40L deficiency). * **Clinical Clue:** Recurrent pyogenic infections (due to low IgG) + *Pneumocystis jirovecii* pneumonia (due to T-cell signaling defect). * **Diagnosis:** Flow cytometry showing absent CD154 on activated T-cells. * **Treatment:** IVIG replacement and Hematopoietic Stem Cell Transplant (HSCT).
Question 542: Which of the following statements regarding IgE antibodies is NOT true?
- A. It mediates the release of histamine and other chemical mediators.
- B. It is the primary antibody involved in allergic reactions.
- C. It is involved in anti-parasitic immune responses.
- D. It can cross the placenta and fix complement. (Correct Answer)
Explanation: ### Explanation The correct answer is **D**, as IgE does **not** cross the placenta nor does it fix complement via the classical pathway. #### Why Option D is the Correct Answer (The False Statement) * **Placental Transfer:** Only **IgG** is capable of crossing the placenta to provide passive immunity to the fetus, due to the presence of specific Fc receptors (FcRn) on placental cells. * **Complement Fixation:** The classical complement pathway is activated by **IgM** (most potent) and **IgG** (subclasses 1, 2, and 3). IgE lacks the binding site for C1q and therefore cannot fix complement. #### Why the Other Options are Incorrect (True Statements) * **Option A & B:** IgE is the primary mediator of **Type I Hypersensitivity** (allergic) reactions. It binds to high-affinity receptors (FcεRI) on **mast cells and basophils**. Upon re-exposure to an allergen, cross-linking of IgE triggers degranulation, releasing histamine, leukotrienes, and prostaglandins. * **Option C:** IgE plays a crucial role in **helminthic (parasitic) infections**. It facilitates Antibody-Dependent Cellular Cytotoxicity (ADCC) by recruiting **eosinophils**, which release major basic protein to destroy the parasite. #### NEET-PG High-Yield Pearls * **Heat Lability:** IgE is the most heat-labile immunoglobulin (inactivated at 56°C for 30 minutes). * **Prausnitz-Küstner (PK) Reaction:** Historically used to detect IgE (reaginic antibody) by passive cutaneous anaphylaxis. * **Serum Levels:** IgE has the lowest serum concentration and the shortest half-life (~2 days) among all immunoglobulins. * **Structure:** It is a monomer with an extra constant domain (**CH4**) on its heavy chain.
Question 543: Which of the following statements is FALSE regarding acquired immunity?
- A. Develops following antigenic exposure
- B. Host cell receptors are specific
- C. Responds to specific microbial antigens
- D. Immunological memory responses are absent (Correct Answer)
Explanation: ### Explanation The correct answer is **D. Immunological memory responses are absent.** This statement is false because **immunological memory** is a hallmark characteristic of acquired (adaptive) immunity, distinguishing it from innate immunity. #### Why Option D is the Correct Answer (The False Statement) Acquired immunity is characterized by the ability to "remember" a specific pathogen. Upon initial exposure (primary response), the body produces **memory B and T cells**. On subsequent exposure to the same antigen (secondary response), these memory cells ensure a faster, more vigorous, and more effective immune attack. In contrast, innate immunity lacks this memory and responds identically to every exposure. #### Why the Other Options are Incorrect (True Statements) * **Option A:** Acquired immunity is not present at birth; it **develops only after exposure** to a foreign antigen (via infection or vaccination). * **Option B:** The receptors on B cells (BCRs) and T cells (TCRs) are **highly specific**. Unlike the broad Pattern Recognition Receptors (PRRs) of innate immunity, these receptors are generated through genetic rearrangement to recognize unique epitopes. * **Option C:** Acquired immunity is **antigen-specific**. It can distinguish between even minor molecular differences in different microbial strains. #### High-Yield Clinical Pearls for NEET-PG * **Components:** Acquired immunity is divided into **Humoral** (B-cells/Antibodies) and **Cell-Mediated** (T-cells). * **Active vs. Passive:** Active immunity (long-lasting, has memory) involves the host's own immune system; Passive immunity (short-acting, no memory) involves the transfer of pre-formed antibodies (e.g., IgA in breast milk, Tetanus antitoxin). * **Lag Period:** Acquired immunity has a distinct lag period during the first exposure, whereas innate immunity is immediate.
Question 544: Mast cells synthesize and/or secrete which of the following substances?
- A. Adrenaline
- B. Acetylcholine
- C. Histamine (Correct Answer)
- D. Heparin
Explanation: **Explanation:** Mast cells are key effector cells of the innate immune system, primarily known for their role in Type I (Immediate) Hypersensitivity reactions. **Why Histamine is the Correct Answer:** Mast cells contain numerous basophilic granules packed with pre-formed inflammatory mediators. Upon activation (cross-linking of IgE receptors), these cells undergo degranulation. **Histamine** is the most significant pre-formed mediator released. It acts on H1 receptors to cause vasodilation, increased vascular permeability (leading to edema), and smooth muscle contraction (bronchospasm). **Analysis of Incorrect Options:** * **Adrenaline (Option A):** This is a hormone and neurotransmitter synthesized by the adrenal medulla and sympathetic nervous system. It is actually the drug of choice to *counteract* mast cell degranulation during anaphylaxis. * **Acetylcholine (Option B):** This is the primary neurotransmitter of the parasympathetic nervous system and neuromuscular junctions, not a secretory product of mast cells. * **Heparin (Option D):** While mast cells *do* contain heparin (an anticoagulant), it serves primarily as a structural matrix for storing histamine within the granules. In the context of standard medical examinations, **Histamine** is the primary functional mediator associated with mast cell clinical manifestations. **High-Yield Clinical Pearls for NEET-PG:** * **Markers:** Tryptase is the most specific marker for mast cell activation (used to diagnose anaphylaxis). * **Receptors:** Mast cells express high-affinity receptors for the Fc portion of IgE (**FcεRI**). * **Location:** They are abundant in tissues exposed to the external environment (skin, GI tract, respiratory tract). * **C-kit (CD117):** This is a crucial surface marker for identifying mast cells in pathology.
Question 545: The technique of immunoblotting used to analyze RNA is named as?
- A. Southern blot
- B. Northern blot (Correct Answer)
- C. Western blot
- D. None of the above
Explanation: **Explanation:** The correct answer is **Northern blot**. In molecular biology, blotting refers to the transfer of biological macromolecules (DNA, RNA, or proteins) from a gel to a carrier membrane for identification. 1. **Why Northern Blot is correct:** This technique is specifically designed to detect and analyze **RNA** sequences. It involves separating RNA samples by size using gel electrophoresis, transferring them to a membrane (like nitrocellulose), and then using a labeled complementary nucleic acid probe to identify specific RNA strands. It is widely used to study gene expression. 2. **Why other options are incorrect:** * **Southern blot:** Named after Edwin Southern, this technique is used for the detection of specific **DNA** sequences. * **Western blot:** This technique is used to identify specific **proteins** using labeled antibodies. It is clinically significant as a confirmatory test for HIV (detecting antibodies against gp120, gp41, and p24). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic (SNOW DROP):** * **S**outhern = **D**NA * **N**orthern = **R**NA * **O** = **O** (No match) * **W**estern = **P**rotein * **Southwestern Blot:** A hybrid technique used to identify **DNA-binding proteins** (e.g., transcription factors like c-Jun and c-Fos). * **Eastern Blot:** Used to analyze post-translational modifications of proteins (e.g., carbohydrates or lipids). * **ELISA vs. Western Blot:** In HIV screening, ELISA is the highly sensitive initial test, while Western Blot is the highly specific confirmatory test.
Question 546: A 21-year-old woman has a history since childhood of recurrent episodes of swelling of the submucosal and subcutaneous tissue of the gastrointestinal and respiratory tracts. Her C1 inhibitor level is less than 5% of the reference value. These findings support a diagnosis of:
- A. DiGeorge syndrome
- B. Hereditary angioedema (Correct Answer)
- C. Nutritional based immune deficiency
- D. Paroxysmal nocturnal hemoglobinuria
Explanation: **Explanation:** The clinical presentation of recurrent, non-pitting edema of the subcutaneous and submucosal tissues (especially the GI tract and airway) without urticaria, combined with a deficiency in **C1 esterase inhibitor (C1-INH)**, is pathognomonic for **Hereditary Angioedema (HAE)**. **Why the correct answer is right:** C1-INH is a serine protease inhibitor that regulates the classical complement pathway and the kinin-generating system. A deficiency leads to the unregulated activation of the kallikrein-kinin cascade, resulting in excessive production of **bradykinin**. Bradykinin increases vascular permeability, leading to the characteristic episodes of swelling. It is inherited in an autosomal dominant fashion. **Why incorrect options are wrong:** * **DiGeorge Syndrome:** A T-cell deficiency caused by 22q11.2 deletion, characterized by thymic hypoplasia, hypocalcemia, and cardiac defects. It does not involve C1-INH. * **Nutritional based immune deficiency:** Usually presents with generalized lymphopenia or specific vitamin/mineral deficiencies (e.g., Zinc) leading to opportunistic infections, not localized angioedema. * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** Caused by a deficiency of GPI-anchored proteins (CD55/CD59) on RBCs, leading to complement-mediated hemolysis and thrombosis, not C1-INH deficiency. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Screen with **C4 levels** (consistently low during and between attacks). Confirm with C1-INH levels/function. * **Management:** Acute attacks are treated with **C1-INH concentrate** or **Icatibant** (bradykinin B2 receptor antagonist). * **Contraindication:** ACE inhibitors are contraindicated as they prevent bradykinin breakdown, worsening the edema. * **Key Distinction:** Unlike allergic angioedema, HAE does **not** present with itching or hives (urticaria).
Question 547: What is the most important cytokine for type II lepra reaction?
- A. IL 1
- B. IL 6
- C. TNF alpha (Correct Answer)
- D. INF gamma
Explanation: **Explanation:** **Type II Lepra Reaction (Erythema Nodosum Leprosum - ENL)** is a classic example of a **Type III Hypersensitivity reaction** (Immune-complex mediated). It typically occurs in patients with multibacillary leprosy (lepromatous or borderline lepromatous) where there is a high bacterial load. **Why TNF-alpha is the correct answer:** TNF-alpha (Tumor Necrosis Factor-alpha) is the central mediator in the pathogenesis of ENL. During the reaction, there is a massive systemic release of TNF-alpha from activated macrophages and monocytes. This cytokine is responsible for the systemic symptoms (fever, malaise) and the acute inflammatory skin lesions. The clinical effectiveness of **Thalidomide** in treating Type II reactions is specifically due to its potent ability to inhibit TNF-alpha synthesis. **Analysis of Incorrect Options:** * **IL-1 and IL-6:** While these are pro-inflammatory cytokines that may be elevated during systemic inflammation, they are secondary mediators and not the primary drivers or therapeutic targets specific to ENL. * **IFN-gamma:** This is the hallmark cytokine of **Type 1 Lepra Reaction** (Reversal Reaction), which involves a Type IV Delayed Hypersensitivity response and a shift toward a Th1 immune profile. **High-Yield Clinical Pearls for NEET-PG:** * **Type I Reaction:** Type IV Hypersensitivity; involves IFN-gamma and IL-2; treated with Steroids. * **Type II Reaction (ENL):** Type III Hypersensitivity; involves TNF-alpha; treated with **Thalidomide** (drug of choice) or Clofazimine. * **Clinical Presentation of ENL:** Tender evanescent subcutaneous nodules, fever, arthralgia, and iridocyclitis. * **Trigger:** Often precipitated by the initiation of Multidrug Therapy (MDT).
Question 548: What region of the immunoglobulin molecule contains the antigen binding site?
- A. Variable region
- B. Hypervariable region (Correct Answer)
- C. Constant region
- D. Idiotype
Explanation: ### Explanation **Correct Answer: B. Hypervariable region** The antigen-binding site (paratope) of an immunoglobulin molecule is specifically located within the **Hypervariable regions** (also known as **Complementarity Determining Regions or CDRs**). While the variable region as a whole provides the structural framework, the hypervariable regions are short stretches of amino acids (three in the light chain and three in the heavy chain) that show the highest degree of sequence variation. These loops come together to form a surface that is chemically and physically complementary to a specific epitope on an antigen. **Analysis of Incorrect Options:** * **A. Variable region:** This is a broader term. The variable (V) region consists of both the hypervariable loops and the relatively stable **framework regions (FRs)**. While the binding site is *within* the variable region, the hypervariable region is the more precise functional unit for binding. * **C. Constant region:** This region (CH and CL) does not bind antigens. It determines the biological properties of the antibody (isotype), such as complement activation and binding to Fc receptors on phagocytes. * **D. Idiotype:** This refers to the *entire set* of antigenic determinants (idiotopes) located in the V region of an antibody. It is a classification of the antibody itself, not the specific binding site. **High-Yield Clinical Pearls for NEET-PG:** * **Papain Digestion:** Cleaves immunoglobulin into **2 Fab fragments** (contain the antigen-binding site) and **1 Fc fragment** (crystallizable). * **Pepsin Digestion:** Cleaves it into **one F(ab')2 fragment** (bivalent) and degraded Fc fragments. * **Hybridoma Technology:** Used to produce monoclonal antibodies that recognize a single specific epitope. * **Isotype Switching:** Involves changes in the **Constant region** of the heavy chain (e.g., IgM to IgG), while the variable region (and thus antigen specificity) remains the same.
Question 549: What is the heterophile agglutination test?
- A. A heterophile antibody that reacts with a microorganism or cells of unrelated species due to common antigen sharing. (Correct Answer)
- B. The test is performed in hypertonic saline (5% saline) or albumin saline.
- C. Coomb, Mourant, and Race devised a reagent: Rabbit anti-human gamma globulin.
- D. Helps to detect the blood group and for cross-matching.
Explanation: **Explanation** **1. Why Option A is Correct:** Heterophile agglutination is based on the principle of **cross-reactivity**. It occurs when antibodies produced against a specific antigen (usually from a pathogen) react with antigens found on the cells of an entirely different species (e.g., sheep, horse, or ox RBCs). This happens because these unrelated species share identical or very similar epitopes, known as **heterophile antigens**. The most classic example is the **Paul-Bunnell Test**, where antibodies produced during Infectious Mononucleosis (EBV) agglutinate sheep erythrocytes. **2. Why Other Options are Incorrect:** * **Option B:** Performing tests in hypertonic or albumin saline is a technique used to detect **"incomplete" or univalent antibodies** (like Rh antibodies), which cannot bridge the gap between RBCs in normal saline. It is not the definition of heterophile agglutination. * **Option C:** This describes the **Antiglobulin (Coombs) Test**. The reagent (Coombs serum) is used to detect antibodies already coated on RBCs, not heterophile cross-reactivity. * **Option D:** While blood grouping involves agglutination, it uses **isoantibodies** (specific to the same species), not heterophile antibodies. **3. NEET-PG High-Yield Clinical Pearls:** * **Paul-Bunnell Test:** Diagnostic for Infectious Mononucleosis (EBV); uses sheep RBCs. * **Weil-Felix Reaction:** A heterophile test for **Rickettsial diseases** where patient serum reacts with *Proteus* antigens (OX-19, OX-2, OX-K). * **Streptococcus MG Agglutination:** Used historically for Primary Atypical Pneumonia (*Mycoplasma pneumoniae*). * **Cold Agglutination Test:** Also seen in *Mycoplasma pneumoniae*, where antibodies agglutinate human O-group RBCs at 4°C.
Question 550: Which of the following is coded by the HLA III gene?
- A. Immunological reaction in graft rejection
- B. Complement (Correct Answer)
- C. Graft versus host reaction
- D. Immunoglobulins
Explanation: The Human Leukocyte Antigen (HLA) complex, located on the short arm of **Chromosome 6**, is divided into three classes. Understanding the distinct functions of these classes is high-yield for NEET-PG. ### **Explanation of the Correct Answer** **Option B (Complement)** is correct because the **HLA Class III** region codes for several secreted proteins involved in the immune response that are *not* cell-surface markers. Specifically, it codes for: * **Complement components:** C2, C4 (C4A and C4B), and Factor B. * **Cytokines:** Tumor Necrosis Factor (TNF-α and TNF-β). * **Heat Shock Proteins (HSP).** Unlike Class I and II, Class III molecules do not participate in antigen presentation but play a vital role in the inflammatory cascade. ### **Analysis of Incorrect Options** * **Options A & C (Graft Rejection / GVHD):** These reactions are primarily mediated by **HLA Class I** (A, B, C) and **HLA Class II** (DR, DQ, DP) molecules. Class I molecules are found on all nucleated cells and are the main targets in acute cellular rejection, while Class II molecules are restricted to antigen-presenting cells and are crucial for T-helper cell activation. * **Option D (Immunoglobulins):** These are produced by B-lymphocytes and are coded by genes located on **Chromosomes 14** (Heavy chains), **2** (Kappa light chains), and **22** (Lambda light chains), not the HLA complex on Chromosome 6. ### **High-Yield Clinical Pearls for NEET-PG** * **Class I HLA:** Coded by A, B, and C loci; presents endogenous antigens to **CD8+ T-cells**. * **Class II HLA:** Coded by DP, DQ, and DR loci; presents exogenous antigens to **CD4+ T-cells**. * **Ankylosing Spondylitis:** Strongly associated with **HLA-B27** (Class I). * **Narcolepsy:** Strongly associated with **HLA-DR2/DQB1*06:02** (Class II). * **Structure:** Class I has one heavy chain and one **β2-microglobulin** (coded on Chromosome 15); Class II has two heavy chains (α and β).
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Cells and Organs of Immune System
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Innate Immunity
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Adaptive Immunity
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Antigens and Antibodies
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Complement System
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Cytokines and Chemokines
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Hypersensitivity Reactions
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Autoimmunity and Autoimmune Diseases
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