Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 21: Tonsils are absent in which of the following conditions?

A. Wiskott-Aldrich syndrome
B. DiGeorge syndrome
C. X linked agammaglobulinemia (Correct Answer)
D. Chediak Higashi syndrome

Explanation: **Explanation:** The correct answer is **X-linked agammaglobulinemia (Bruton’s Tyrosine Kinase deficiency)**. **Why X-linked agammaglobulinemia (XLA) is the correct answer:** XLA is characterized by a mutation in the **BTK gene**, which is essential for the maturation of B-cells. In this condition, B-cell development is arrested at the pre-B stage in the bone marrow. Consequently, there is a profound deficiency of mature B-lymphocytes and all classes of immunoglobulins. Since **tonsils and Peyer’s patches** are secondary lymphoid organs composed primarily of B-cell follicles and germinal centers, their development is severely stunted. The **absence of palpable tonsils** and lymph nodes is a classic clinical sign of XLA. **Analysis of Incorrect Options:** * **Wiskott-Aldrich Syndrome:** This is a triad of eczema, thrombocytopenia, and immunodeficiency. While it involves T and B cell dysfunction, lymphoid tissue (like tonsils) is generally present, though it may atrophy over time. * **DiGeorge Syndrome:** This is a **T-cell deficiency** caused by the failure of the 3rd and 4th pharyngeal pouches to develop. While the **thymus** is absent or hypoplastic, B-cell areas (and thus tonsils) are typically present, although their function may be impaired due to lack of T-cell help. * **Chediak-Higashi Syndrome:** This is a defect in **lysosomal trafficking** (LYST gene) affecting phagocytes. It presents with partial albinism and giant granules in neutrophils; it does not result in the absence of tonsillar tissue. **High-Yield Clinical Pearls for NEET-PG:** * **XLA Clinical Presentation:** Recurrent pyogenic infections (e.g., *S. pneumoniae*, *H. influenzae*) starting after 6 months of age (once maternal IgG wanes). * **Diagnostic Hallmark:** Absent/low B-cells (CD19+, CD20+) on flow cytometry and low levels of all Ig classes. * **Live Vaccines:** Strictly contraindicated in XLA (especially OPV) due to the risk of vaccine-associated paralytic poliomyelitis.

Question 22: To fully activate a naive CD4 T cell, what must the antigen-presenting cell express?

A. MHC class I and class II molecules
B. Interleukin-2
C. B7 and MHC class II molecules (Correct Answer)
D. CD28 and MHC class II molecules

Explanation: ### Explanation To activate a naive CD4+ T cell, a **two-signal model** is required. This ensures that the immune system does not mount an accidental response against self-antigens. 1. **Signal 1 (Antigen Recognition):** The T-cell receptor (TCR) on the CD4 cell recognizes the specific peptide fragment presented by the **MHC Class II** molecule on the surface of a professional Antigen-Presenting Cell (APC) like a dendritic cell, macrophage, or B cell. 2. **Signal 2 (Co-stimulation):** This is the "confirmation" signal. The **B7 protein** (CD80/86) on the APC binds to the **CD28** receptor on the T cell. Without this interaction, the T cell becomes "anergic" (non-responsive). **Analysis of Options:** * **Option A:** MHC Class I is present on all nucleated cells and presents to CD8+ T cells, not CD4+ cells. * **Option B:** Interleukin-2 (IL-2) is a cytokine produced *by* the T cell after activation to promote clonal expansion; it is not expressed by the APC to initiate activation. * **Option D:** CD28 is located on the **T cell**, not the APC. The question asks what the **APC** must express. **High-Yield Clinical Pearls for NEET-PG:** * **Signal 1:** TCR + MHC II (CD4) or MHC I (CD8). * **Signal 2:** CD28 (T cell) + B7 (APC). * **Anergy:** If Signal 1 occurs without Signal 2, the T cell enters a state of prolonged inactivation. * **CTLA-4:** A molecule on T cells that binds B7 with higher affinity than CD28 but sends an *inhibitory* signal, acting as a "brake" on the immune response (target of checkpoint inhibitors in cancer).

Question 23: HLA typing is useful in:

A. Blood grouping
B. Assessing prognosis of disease
C. Cancer therapy
D. Cases of parental dispute (Correct Answer)

Explanation: **Explanation:** **HLA (Human Leukocyte Antigen)** typing, also known as tissue typing, identifies the specific MHC (Major Histocompatibility Complex) proteins on the surface of cells. These antigens are highly polymorphic and are inherited in a Mendelian codominant fashion (one haplotype from each parent). **Why Option D is Correct:** Because of the extreme diversity (polymorphism) of HLA alleles, the probability of two unrelated individuals having the same HLA profile is exceptionally low. Since a child must inherit one HLA haplotype from each biological parent, HLA typing serves as a powerful tool in **paternity testing and resolving parental disputes**. If a child possesses an HLA antigen not present in either the mother or the alleged father, that man is excluded as the biological father. **Why Other Options are Incorrect:** * **A. Blood Grouping:** This is determined by ABO and Rh antigens on RBCs, not HLA (which are primarily on nucleated cells). * **B. Assessing Prognosis:** While certain HLA types are associated with disease *susceptibility* (e.g., HLA-B27 and Ankylosing Spondylitis), they are generally used for diagnosis or risk assessment rather than predicting the clinical prognosis of an established disease. * **C. Cancer Therapy:** While HLA matching is vital for Bone Marrow Transplants (to prevent GVHD), it is not a standard "therapy" for cancer itself. **High-Yield Clinical Pearls for NEET-PG:** * **MHC Location:** Encoded on the short arm of **Chromosome 6**. * **Organ Transplantation:** HLA-DR matching is the most important for successful renal transplant, followed by HLA-B and HLA-A. * **Key HLA-Disease Associations:** * **HLA-B27:** Ankylosing Spondylitis, Reiter’s syndrome. * **HLA-DR3/DR4:** Type 1 Diabetes Mellitus. * **HLA-DQ2/DQ8:** Celiac Disease. * **HLA-B51:** Behcet’s Disease.

Question 24: Epstein-Barr virus (EBV) VCA-IgG 1:80 and EBV antibody to early antigen EA1:320 suggest which one of the following diseases?

A. Chronic infectious mononucleosis (Correct Answer)
B. Primary syphilis
C. Scarlet fever
D. Primary atypical pneumonia

Explanation: ### Explanation **Correct Option: A. Chronic infectious mononucleosis** The diagnosis of Epstein-Barr Virus (EBV) infection relies on the interpretation of specific antibody profiles. * **VCA-IgG (Viral Capsid Antigen):** These antibodies appear in the acute phase, peak at 2–4 weeks, and persist for life. A titer of 1:80 indicates past or ongoing exposure. * **EA (Early Antigen):** These antibodies are typically markers of **active viral replication**. EA-D (diffuse) usually disappears after recovery. However, persistently high titers (like 1:320) or a reappearance of EA antibodies are classic indicators of **Chronic Active EBV infection** or reactivation. * In this case, the significantly elevated EA titer (1:320) relative to the VCA-IgG suggests that the virus is actively replicating over a prolonged period, pointing toward Chronic Infectious Mononucleosis. **Why Incorrect Options are Wrong:** * **B. Primary Syphilis:** Caused by *Treponema pallidum*. Diagnosis is made via dark-field microscopy of chancre fluid or serology (VDRL/RPR and FTA-ABS), not EBV titers. * **C. Scarlet Fever:** Caused by *Streptococcus pyogenes* (Group A Strep) erythrogenic toxin. Diagnosis is clinical (strawberry tongue, sandpaper rash) and confirmed by rapid antigen detection or throat culture. * **D. Primary Atypical Pneumonia:** Most commonly caused by *Mycoplasma pneumoniae*. Diagnosis involves **Cold Agglutinins** or PCR, not EBV serology. **High-Yield Clinical Pearls for NEET-PG:** * **Heterophile Antibodies (Monospot Test):** Positive in Infectious Mononucleosis (IM) but negative in CMV-induced IM-like syndrome. * **EBNA (EBV Nuclear Antigen):** These antibodies appear only *after* the acute phase (3–4 months later). Their **absence** in the presence of VCA-IgG suggests an acute/recent infection. * **Atypical Lymphocytes (Downey Cells):** Activated T-cells seen on peripheral smear in EBV infection. * **Associations:** EBV is linked to Burkitt Lymphoma (t8;14), Nasopharyngeal Carcinoma, and Oral Hairy Leukoplakia in HIV patients.

Question 25: Which Toll-like receptor (TLR) is present on flagella of bacteria?

A. TLR-1
B. TLR-3
C. TLR-5 (Correct Answer)
D. TLR-7

Explanation: **Explanation:** Toll-like receptors (TLRs) are a class of **Pattern Recognition Receptors (PRRs)** that play a crucial role in the innate immune system by detecting **Pathogen-Associated Molecular Patterns (PAMPs)**. **Why TLR-5 is correct:** TLR-5 is specifically designed to recognize **Flagellin**, the principal protein component of bacterial flagella. This receptor is primarily expressed on the surface of epithelial cells, monocytes, and dendritic cells. When flagellin binds to TLR-5, it triggers a signaling cascade (via the MyD88 pathway) that leads to the activation of NF-κB, resulting in the production of pro-inflammatory cytokines. **Analysis of Incorrect Options:** * **TLR-1:** Typically forms a heterodimer with TLR-2 to recognize **triacyl lipopeptides** found in bacteria and mycobacteria. * **TLR-3:** Located on endosomal membranes; it specifically recognizes **double-stranded RNA (dsRNA)**, which is a hallmark of viral replication. * **TLR-7:** Also located in endosomes; it recognizes **single-stranded RNA (ssRNA)** from viruses (similar to TLR-8). **High-Yield Clinical Pearls for NEET-PG:** * **TLR-4:** Recognizes **Lipopolysaccharide (LPS)** of Gram-negative bacteria (requires MD2 and CD14 co-receptors). This is a very frequent exam topic. * **TLR-2:** Recognizes **Peptidoglycan** and Lipoteichoic acid (Gram-positive bacteria). * **TLR-9:** Recognizes unmethylated **CpG DNA** motifs common in bacteria and viruses. * **Location Tip:** TLRs 1, 2, 4, 5, and 6 are found on the **cell surface** (detecting extracellular pathogens), while TLRs 3, 7, 8, and 9 are found in **endosomes** (detecting intracellular/nucleic acid PAMPs).

Question 26: All of the following bacterial proteins are secreted from the primary granules of neutrophils except:

A. Bacterial cell permeability protein
B. Defensins
C. Lysozyme
D. Lactoferrin (Correct Answer)

Explanation: **Explanation:** The correct answer is **Lactoferrin**. Neutrophils contain two main types of granules—**Primary (Azurophilic)** and **Secondary (Specific)**—which house different antimicrobial proteins essential for intracellular killing. 1. **Why Lactoferrin is the correct answer:** Lactoferrin is a characteristic marker of **Secondary (Specific) granules**. It acts by sequestering iron, an essential nutrient for bacterial growth, thereby exerting a bacteriostatic effect. Since the question asks for proteins secreted from *primary* granules *except* one, Lactoferrin is the outlier. 2. **Analysis of Incorrect Options (Primary Granule components):** * **Bacterial permeability-increasing (BPI) protein:** Found in primary granules; it highly targets Gram-negative bacteria by binding to LPS. * **Defensins:** These are cationic proteins found in primary granules that create pores in bacterial membranes. * **Lysozyme:** This enzyme is unique because it is found in **both** primary and secondary granules. Since it is present in primary granules, it is not the "except" answer. It works by cleaving the glycan backbone of peptidoglycan. **High-Yield Clinical Pearls for NEET-PG:** * **Primary (Azurophilic) Granules:** Contain **Myeloperoxidase (MPO)** (the most specific marker), BPI, Defensins, Elastase, and Lysozyme. * **Secondary (Specific) Granules:** Contain **Lactoferrin**, Vitamin B12-binding protein, Collagenase, and Lysozyme. * **Mnemonic for Primary:** "B-L-E-D" (BPI, Lysozyme, Elastase, Defensins) + MPO. * **Clinical Correlation:** In **Chediak-Higashi Syndrome**, there is a defect in lysosomal trafficking leading to giant azurophilic granules, resulting in impaired chemotaxis and degranulation.

Question 27: What is the primary antibody involved in cold agglutinin disease?

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

Explanation: ### Explanation **Correct Option: D (IgM)** Cold agglutinin disease (CAD) is a type of autoimmune hemolytic anemia (AIHA) caused by **IgM antibodies**. These antibodies are called "cold" because they have maximal binding affinity at low temperatures (typically 0°C to 4°C). **The Mechanism:** IgM is a large pentameric molecule. When blood circulates through cooler peripheral areas (like fingers, toes, or ears), IgM binds to the **I antigen** on the surface of Red Blood Cells (RBCs). This binding activates the **Classical Complement Pathway**. While the IgM often dissociates when the blood warms back up in the core circulation, the **C3b** complement fragment remains attached to the RBC, leading to extravascular hemolysis primarily in the liver. **Why other options are incorrect:** * **IgG (Option B):** IgG is the primary antibody in **Warm AIHA**. IgG reacts best at body temperature (37°C) and typically targets the Rh antigen. It leads to splenic sequestration (extravascular hemolysis). * **IgA (Option A):** While IgA is the primary secretory antibody found in mucosal surfaces, it is rarely involved in autoimmune hemolytic anemias. * **IgE (Option C):** IgE is primarily involved in Type I hypersensitivity reactions (allergies) and parasitic infections; it does not play a role in cold agglutinin disease. **High-Yield Clinical Pearls for NEET-PG:** * **Associations:** Acute CAD is often seen following **Mycoplasma pneumoniae** infection or **Infectious Mononucleosis (EBV)**. Chronic CAD is associated with B-cell lymphoproliferative disorders. * **Peripheral Smear:** Characterized by **RBC clumping/agglutination** (unlike the rouleaux formation seen in Multiple Myeloma). * **Direct Coombs Test:** Will be positive for **C3d** but negative for IgG. * **Clinical Presentation:** Patients may experience **acrocyanosis** (bluish discoloration of extremities) upon exposure to cold.

Question 28: Toxoid is prepared from which of the following?

A. Exotoxin (Correct Answer)
B. Endotoxin
C. Both
D. None

Explanation: **Explanation:** **1. Why Exotoxin is Correct:** A **toxoid** is a bacterial toxin whose toxicity has been inactivated (usually by treatment with formaldehyde, heat, or aging) while its **immunogenicity** remains intact. Only **exotoxins**—which are soluble proteins secreted by living bacteria—can be converted into toxoids. Because exotoxins are highly antigenic proteins, they can be modified to lose their poisonous effect while still stimulating the B-cells to produce protective antibodies (antitoxins). **2. Why Other Options are Incorrect:** * **Endotoxins (Option B):** These are lipopolysaccharides (LPS) found in the outer membrane of Gram-negative bacteria. Unlike exotoxins, endotoxins are heat-stable and poorly antigenic. They cannot be effectively detoxified to form toxoids while retaining the ability to induce a protective immune response. * **Both (Option C):** Since endotoxins cannot form toxoids, this option is incorrect. **3. NEET-PG High-Yield Clinical Pearls:** * **Common Toxoid Vaccines:** The most classic examples are **Tetanus toxoid** (*Clostridium tetani*) and **Diphtheria toxoid** (*Corynebacterium diphtheriae*). * **Type of Immunity:** Toxoids induce **Active Immunity**. * **Key Difference:** Exotoxins are typically produced by both Gram-positive and Gram-negative bacteria and are highly potent (e.g., Botulinum), whereas endotoxins are specific to Gram-negative bacteria and are generally less potent but trigger systemic inflammatory responses (septic shock). * **Formaldehyde (Formalin):** This is the most common agent used in the laboratory to convert a toxin into a toxoid.

Question 29: Which statement is false about haptens?

A. Haptens are low molecular weight molecules (Correct Answer)
B. Haptens lack immunogenicity
C. Haptens retain antigenicity
D. Complex haptens contain two or more epitopes

Explanation: **Explanation** The question asks for the **false** statement regarding haptens. However, based on standard immunological principles, **Option A is actually a true statement**, as haptens are defined as low molecular weight molecules. In the context of NEET-PG, this question often appears where the intended "false" statement relates to the functional definition of haptens versus complete antigens. **1. Why Option A is the "Correct" Answer (Identifying the Falsehood):** In many standardized exams, if Option A is marked as the "false" statement, it is usually a technical error in the question key or a nuance regarding "Complex Haptens." However, scientifically, **Haptens are indeed low molecular weight (<10,000 Daltons)**. If this were a "select the false statement" question, all options A, B, and C are technically true. If Option A is the keyed answer, it implies the examiner considers haptens to be of variable weight, though this contradicts standard textbooks like Ananthanarayan. **2. Analysis of Other Options:** * **Option B (True):** Haptens **lack immunogenicity**. They cannot induce an immune response on their own because they are too small to cross-link B-cell receptors or be processed for T-cell presentation. * **Option C (True):** Haptens **retain antigenicity**. They can react specifically with antibodies once those antibodies have been formed (usually after the hapten was conjugated to a carrier protein). * **Option D (True):** **Complex haptens** are polyvalent (contain two or more epitopes) and can precipitate with specific antibodies, whereas **Simple haptens** are univalent and cannot form a precipitate (they only inhibit precipitation). **High-Yield Clinical Pearls for NEET-PG:** * **Hapten + Carrier = Complete Antigen:** A hapten becomes immunogenic only when covalently bound to a large protein carrier (e.g., Albumin). * **Clinical Example:** **Penicillin** is a classic hapten. It is too small to be immunogenic alone, but when it binds to serum proteins, it becomes a complete antigen, potentially leading to Type I Hypersensitivity (Anaphylaxis). * **Landsteiner’s Experiments:** Much of our knowledge of antigenic specificity comes from Karl Landsteiner’s work using haptens.

Question 30: Which of the following is NOT a function of complements?

A. Cell lysis
B. Antiviral action
C. Promotes phagocytosis
D. Toxin neutralization (Correct Answer)

Explanation: The complement system is a biochemical cascade of the innate immune system that helps clear pathogens. However, it lacks the structural ability to neutralize toxins. ### **Why Toxin Neutralization is the Correct Answer** **Toxin neutralization** is primarily a function of **antibodies** (specifically IgG and IgA). Antibodies bind to the active sites of toxins or block their entry into host cells. The complement system consists of plasma proteins that act on cell surfaces or viral envelopes but cannot chemically modify or "neutralize" small soluble protein toxins. ### **Explanation of Other Options** * **Cell Lysis (Option A):** This is a primary function mediated by the **Membrane Attack Complex (MAC)**, consisting of C5b-C9. It creates pores in the lipid bilayer of Gram-negative bacteria and infected cells, leading to osmotic lysis. * **Antiviral Action (Option B):** Complements contribute to antiviral immunity by opsonizing viral particles (C3b), promoting their phagocytosis, and directly lysing enveloped viruses via the MAC. * **Promotes Phagocytosis (Option C):** This occurs through **Opsonization**. **C3b** (and C4b) acts as a major opsonin, coating the pathogen surface. Phagocytes (neutrophils/macrophages) have CR1 receptors that bind to C3b, significantly enhancing the engulfment of the pathogen. ### **High-Yield Clinical Pearls for NEET-PG** * **C3b:** The most potent **Opsonin**. * **C5a:** The most potent **Chemotactic agent** and Anaphylatoxin. * **C5b-9:** The **Membrane Attack Complex (MAC)**; deficiency leads to recurrent *Neisseria* infections. * **C1 Esterase Inhibitor Deficiency:** Leads to **Hereditary Angioedema** (due to overproduction of bradykinin). * **CH50 Assay:** Used to screen for deficiencies in the Classical Pathway.

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Immunology — MCQs

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