Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 261: Transfer factor is an example of which type of immunity?

A. Innate immunity
B. Adoptive immunity (Correct Answer)
C. Natural active immunity
D. Artificial active immunity

Explanation: **Explanation:** **Adoptive immunity** refers to the transfer of pre-formed immune components (specifically lymphocytes or their products) from a sensitized donor to a non-immune recipient to provide immediate, specific cell-mediated immunity (CMI). **Transfer factor**, discovered by Sherwood Lawrence, is a low-molecular-weight extract derived from sensitized T-lymphocytes. When injected, it "teaches" the recipient's naive T-cells to recognize and respond to specific antigens, effectively transferring delayed-type hypersensitivity. **Why other options are incorrect:** * **Innate immunity:** This is the non-specific, first-line defense present from birth (e.g., skin, neutrophils). It does not involve the transfer of sensitized lymphocyte products. * **Natural active immunity:** This occurs when a person is naturally exposed to a live pathogen and their own immune system develops a response (e.g., recovering from Measles). * **Artificial active immunity:** This is induced by intentional exposure to antigens through vaccination (e.g., BCG or Hepatitis B vaccine), where the body actively produces its own antibodies and T-cells. **High-Yield NEET-PG Pearls:** * **Transfer Factor:** It is heat-stable, non-antigenic, and dialyzable. It is used clinically in treating immunodeficiency states (like Wiskott-Aldrich syndrome) and certain chronic infections (like mucocutaneous candidiasis). * **Adoptive Immunity vs. Passive Immunity:** While both provide immediate protection, "Passive" usually refers to the transfer of **antibodies** (e.g., Rabies IG), whereas "Adoptive" refers to the transfer of **cells or cell-mediated factors**. * Other examples of Adoptive Immunity include **Bone Marrow Transplantation** and **CAR-T cell therapy**.

Question 262: Which of the following is associated with HLA B27?

A. Autoimmune diseases
B. Graft rejection
C. Cell-mediated cytolysis of viral-infected cells
D. Ankylosing spondylitis (Correct Answer)

Explanation: **Explanation:** **Ankylosing Spondylitis (Option D)** is the correct answer because it has the strongest known association with the **HLA-B27** allele. HLA-B27 is a Class I Human Leukocyte Antigen (MHC Class I). Over 90% of patients with Ankylosing Spondylitis test positive for HLA-B27, making it a classic example of an MHC-disease association. **Analysis of Incorrect Options:** * **Autoimmune diseases (Option A):** While many autoimmune diseases are linked to HLA, they are more commonly associated with **MHC Class II** alleles (e.g., HLA-DR3/DR4 in Type 1 Diabetes or Rheumatoid Arthritis). HLA-B27 is specifically linked to Seronegative Spondyloarthropathies. * **Graft rejection (Option B):** This is a general process mediated by mismatching of various HLA antigens (both Class I and II) between donor and recipient, rather than a specific association with the B27 allele. * **Cell-mediated cytolysis (Option C):** This is the *physiological function* of all MHC Class I molecules (presenting endogenous antigens to CD8+ T-cells). While HLA-B27 performs this function, it is not uniquely "associated" with it more than any other Class I molecule. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic (PAIR):** HLA-B27 is associated with **P**soriatic arthritis, **A**nkylosing spondylitis, **I**nflammatory bowel disease-associated arthritis, and **R**eactive arthritis (formerly Reiter’s syndrome). * **Molecular Mimicry:** The pathogenesis is often linked to cross-reactivity between HLA-B27 and bacterial antigens (e.g., *Klebsiella*). * **Other HLA Associations:** * **HLA-B51:** Behcet’s disease. * **HLA-DR3:** SLE, Myasthenia Gravis. * **HLA-DQ2/DQ8:** Celiac disease.

Question 263: Complement components are primarily which type of molecule?

A. Lipoproteins
B. Glycoproteins (Correct Answer)
C. Polysaccharides
D. Lipids

Explanation: **Explanation:** **1. Why Glycoproteins are Correct:** The complement system consists of over 30 circulating and membrane-bound proteins that act as a cascade to mediate inflammation and pathogen lysis. Chemically, almost all complement components (such as C1 through C9) are **glycoproteins**. They are synthesized primarily by the **liver** (hepatocytes), though significant amounts are also produced by macrophages, monocytes, and epithelial cells in the genitourinary and gastrointestinal tracts. These proteins circulate in the blood as inactive precursors (zymogens) until they are triggered by specific pathways (Classical, Alternative, or Lectin). **2. Why Other Options are Incorrect:** * **Lipoproteins (A):** These are complexes of lipids and proteins (like LDL or HDL) used for lipid transport. Complement factors do not have a primary lipid-transport structure. * **Polysaccharides (C):** These are complex carbohydrates (like glycogen or bacterial capsules). While complement proteins contain carbohydrate chains (making them glycoproteins), their backbone is polypeptide-based. * **Lipids (D):** Lipids are hydrophobic molecules (fats/oils). Complement factors are water-soluble proteins found in the serum. **3. NEET-PG High-Yield Pearls:** * **Site of Synthesis:** Liver is the primary source. (Exception: C1 is synthesized by intestinal epithelium). * **Heat Lability:** Complement is **heat-labile**; it is inactivated by heating serum at **56°C for 30 minutes**. * **Most Abundant:** **C3** is the complement component present in the highest concentration in the serum. * **Acute Phase Reactants:** Many complement proteins act as positive acute-phase reactants, increasing during acute inflammation. * **Electrophoresis:** On serum electrophoresis, most complement components migrate in the **Beta-globulin** fraction.

Question 264: Natural Killer (NK) cells are components of which system?

A. Innate immunity (Correct Answer)
B. Acquired immunity
C. Adaptive immunity
D. None of the above

Explanation: **Explanation:** **Why Innate Immunity is Correct:** Natural Killer (NK) cells are large granular lymphocytes that serve as the first line of defense against virally infected cells and tumor cells. They are classified under **Innate Immunity** because they lack antigen-specific receptors (like TCR or BCR). Instead, they use a "germline-encoded" recognition system involving **Inhibitory Receptors** (which recognize MHC-I on healthy cells) and **Activating Receptors** (which recognize stress-induced ligands). When a cell loses MHC-I expression (a common viral/tumor escape mechanism), the NK cell is no longer inhibited and triggers apoptosis via perforins and granzymes. **Why Other Options are Incorrect:** * **Acquired/Adaptive Immunity (Options B & C):** These terms are synonymous. Adaptive immunity relies on T and B lymphocytes which require gene rearrangement to create highly specific receptors and generate immunological memory. While NK cells share a common lymphoid progenitor with T/B cells, they do not undergo receptor rearrangement and do not typically produce a memory response in the classical sense. **High-Yield Clinical Pearls for NEET-PG:** * **Marker of NK Cells:** CD56 (NCAM) and CD16 (FcγRIII) are the definitive surface markers. * **Mechanism of Action:** They induce apoptosis through the **Perforin-Granzyme pathway** and **Fas-FasL interaction**. * **Cytokine Stimulation:** Their activity is significantly enhanced by **IL-2, IL-12, IL-15, and IFN-α/β**. * **Antibody-Dependent Cellular Cytotoxicity (ADCC):** NK cells mediate ADCC via the CD16 receptor, which binds to the Fc portion of IgG coated on target cells. * **MHC Paradox:** Unlike Cytotoxic T-cells (CD8+), which require MHC-I to "see" an antigen, NK cells are activated by the **absence or downregulation of MHC-I** ("Missing Self" hypothesis).

Question 265: Epstein Barr virus causes autoimmunity by which mechanism?

A. Molecular Mimicry
B. Release of Sequestrated Antigen
C. Inappropriate Expression of MHC Class II Molecules
D. Polyclonal B cell Activation (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Polyclonal B cell Activation** **Mechanism:** Epstein-Barr Virus (EBV) is a potent **polyclonal B-cell activator**. The virus binds to the **CD21** receptor (CR2) on B-lymphocytes. Once inside, it bypasses the need for T-cell help and directly triggers the proliferation of numerous B-cell clones. This massive, non-specific activation leads to the production of various antibodies, including **autoantibodies** (e.g., rheumatoid factor, cold agglutinins) and the characteristic **heterophile antibodies** used for diagnosis (Monospot test). Because these B-cells produce antibodies against self-antigens without specific antigenic stimulation, it leads to transient or chronic autoimmunity. **Why other options are incorrect:** * **A. Molecular Mimicry:** This occurs when microbial antigens share structural similarities with self-antigens (e.g., *S. pyogenes* M-protein and cardiac myosin in Rheumatic Fever). While EBV has some mimicry roles, its primary, hallmark mechanism is polyclonal activation. * **B. Release of Sequestrated Antigen:** This refers to the exposure of antigens normally hidden from the immune system (e.g., lens antigen after eye trauma or sperm after vasectomy). EBV does not primarily act through this mechanism. * **C. Inappropriate Expression of MHC Class II:** This occurs when cells that normally don't express MHC II (like pancreatic beta cells or thyroid cells) start doing so, often induced by IFN-gamma, leading to self-antigen presentation. This is seen in Type 1 Diabetes and Graves' disease. **High-Yield Facts for NEET-PG:** * **EBV Receptor:** CD21 (also the receptor for C3d). * **Atypical Lymphocytes:** These are **CD8+ T-cells** (Downey cells) reacting against the infected B-cells. * **Associated Malignancies:** Burkitt Lymphoma (t 8;14), Nasopharyngeal Carcinoma, and Hodgkin Lymphoma (Mixed cellularity type). * **Classic Triad:** Fever, Pharyngitis, and Lymphadenopathy.

Question 266: Which of the following cell surface markers is required for lysis of IgG-coated target cells (antibody-dependent, cell-mediated cytotoxicity, or ADCC) by natural killer cells?

A. CD3
B. CD16 (Correct Answer)
C. CD19
D. CD21

Explanation: ### Explanation **Correct Option: B (CD16)** Natural Killer (NK) cells mediate **Antibody-Dependent Cell-mediated Cytotoxicity (ADCC)** by recognizing and binding to target cells coated with IgG antibodies. This process is specifically mediated by **CD16**, which is a low-affinity receptor for the **Fc portion of IgG (FcγRIII)**. When CD16 binds to the Fc region of the antibody attached to a target cell (e.g., a virus-infected or tumor cell), it triggers the NK cell to release perforins and granzymes, leading to apoptosis of the target. **Analysis of Incorrect Options:** * **CD3 (Option A):** This is a definitive marker for **T-lymphocytes**. It is part of the T-cell receptor (TCR) complex involved in signal transduction. NK cells are "null cells" (CD3 negative). * **CD19 (Option C):** This is a major surface marker for **B-lymphocytes**, present from the pro-B cell stage until just before differentiation into plasma cells. It plays a role in B-cell activation. * **CD21 (Option D):** Also known as Complement Receptor 2 (CR2), it is found on **B-cells**. It is the receptor for the C3d complement fragment and notably serves as the attachment site for the **Epstein-Barr Virus (EBV)**. **High-Yield Clinical Pearls for NEET-PG:** * **NK Cell Markers:** The most specific markers for identifying NK cells in flow cytometry are **CD56** (adhesion molecule) and **CD16**. * **MHC-I Relationship:** NK cells kill cells that lack **MHC Class I** expression (the "Missing Self" hypothesis), a common tactic used by viruses and tumors to evade Cytotoxic T-cells (CD8+). * **ADCC Mechanism:** Besides NK cells, other cells capable of ADCC include macrophages, neutrophils, and eosinophils (the latter specifically against helminths via IgE).

Question 267: MHC class II antigens are located on which of the following cells?

A. Platelets
B. Dendritic cells (Correct Answer)
C. RBCs
D. T-cells

Explanation: ### Explanation **MHC Class II** molecules are essential for the exogenous pathway of antigen presentation. They are constitutively expressed only on **Professional Antigen-Presenting Cells (pAPCs)**. **Why Dendritic Cells (Option B) is Correct:** Dendritic cells are the most potent professional APCs. Their primary role is to capture exogenous antigens, process them into peptides, and present them via **MHC Class II** molecules to **CD4+ T-helper cells**. Other professional APCs include B-cells and Macrophages. **Why Other Options are Incorrect:** * **Platelets (Option A) & RBCs (Option C):** MHC molecules are generally expressed on nucleated cells. Since RBCs and platelets are non-nucleated, they lack MHC expression. Specifically, RBCs lack MHC Class I, which is why they are not targets for cytotoxic T-cells (important in malaria and blood transfusions). * **T-cells (Option D):** Resting T-cells express **MHC Class I** (found on all nucleated cells) but do *not* express MHC Class II. However, human T-cells can express MHC Class II only upon **activation**. In the context of standard medical exams, T-cells are categorized as recipients of MHC presentation, not the primary carriers of MHC II. --- ### High-Yield Clinical Pearls for NEET-PG: * **MHC Restriction:** MHC Class I presents to CD8+ (Cytotoxic) T-cells, while MHC Class II presents to CD4+ (Helper) T-cells (Rule of 8: 1×8=8; 2×4=8). * **Genetic Loci:** In humans, MHC is known as HLA (Human Leukocyte Antigen). MHC Class I is encoded by HLA-A, B, and C; MHC Class II is encoded by **HLA-DP, DQ, and DR**. * **Structure:** MHC II is a heterodimer consisting of an **α chain and a β chain**, both of which are polymorphic and span the cell membrane. * **Invariant Chain (Ii):** This protein prevents endogenous peptides from binding to MHC II in the endoplasmic reticulum, ensuring it only binds exogenous antigens in the endosome.

Question 268: What aspect of the relevant condition is tested by the lepromine test?

A. Cell mediated immunity (Correct Answer)
B. Infectivity
C. Diagnosis
D. None

Explanation: The **Lepromin test** is a skin test used to assess the host’s specific **Cell-Mediated Immunity (CMI)** against *Mycobacterium leprae*. It is not a diagnostic tool but a prognostic one. ### **Explanation of Options** * **A. Cell-Mediated Immunity (Correct):** The test involves the intradermal injection of lepromin (antigen derived from killed *M. leprae*). A positive reaction indicates a robust delayed-type hypersensitivity (DTH) response, signifying that the patient’s CMI is intact and capable of limiting the infection. * **B. Infectivity:** The test does not measure the bacterial load or the ability of the patient to transmit the disease. Infectivity is usually assessed via the **Bacteriological Index (BI)** from skin smears. * **C. Diagnosis:** The Lepromin test is **not used for diagnosis** because it can be positive in healthy individuals (due to cross-reactivity with BCG or other mycobacteria) and is often negative in the most severe form of the disease (lepromatous leprosy). Diagnosis is clinical and confirmed by slit-skin smears or biopsy. ### **High-Yield Clinical Pearls for NEET-PG** 1. **Two Types of Reactions:** * **Fernandez Reaction:** Early (48 hours); indicates a non-specific hypersensitivity. * **Mitsuda Reaction:** Late (3–4 weeks); indicates specific CMI. A nodule >5mm is positive. 2. **Prognostic Value:** * **Tuberculoid (TT) Leprosy:** Lepromin test is **strongly positive** (High CMI). * **Lepromatous (LL) Leprosy:** Lepromin test is **negative** (Deficient CMI). 3. **Classification:** It helps in classifying the type of leprosy and determining the stability of the disease. A shift from negative to positive indicates clinical improvement.

Question 269: Which of the following bodily secretions contains IgA?

A. Tears and saliva (Correct Answer)
B. Cerebrospinal fluid
C. Hairs
D. Vaginal fluid

Explanation: **Explanation:** **Immunoglobulin A (IgA)** is the primary antibody class associated with **mucosal immunity**. Specifically, **Secretory IgA (sIgA)** is the predominant isotype found in external secretions that bathe mucosal surfaces. 1. **Why Option A is correct:** IgA is synthesized by plasma cells in the lamina propria and transported across epithelial cells into secretions. It is found in high concentrations in **tears, saliva, colostrum (first milk), nasal mucus, and gastrointestinal/genitourinary secretions**. Its primary role is "immune exclusion"—preventing the attachment of bacteria and viruses to mucosal surfaces. 2. **Why other options are incorrect:** * **Cerebrospinal fluid (CSF):** Under normal physiological conditions, CSF contains very low levels of proteins and immunoglobulins due to the blood-brain barrier. * **Hairs:** Hair consists of keratinized dead cells and does not contain active immunoglobulins. * **Vaginal fluid:** While vaginal fluid *does* contain some IgA, it is predominantly characterized by **IgG** (derived from systemic circulation). In the context of standard medical examinations, tears and saliva are the classic, high-yield examples of IgA-rich fluids. **High-Yield Clinical Pearls for NEET-PG:** * **Structure:** IgA exists as a **monomer** in serum but as a **dimer** in secretions. * **The J-Chain:** Holds the two IgA monomers together. * **Secretory Component:** A polypeptide produced by epithelial cells that protects sIgA from digestion by proteolytic enzymes in the gut/saliva. * **Selective IgA Deficiency:** The most common primary immunodeficiency; patients often present with recurrent sinopulmonary and GI infections. * **Milk:** IgA provides passive natural immunity to the neonate via breast milk.

Question 270: Killer cells and helper cells are components of which cell type?

A. B cells
B. T cells (Correct Answer)
C. Monocytes
D. Macrophage

Explanation: ### Explanation **Correct Answer: B. T cells** **Concept:** T lymphocytes (T cells) are the primary mediators of cell-mediated immunity. They are categorized into distinct functional subsets based on their surface markers (CD markers) and roles in the immune response: 1. **Helper T cells (Th cells):** Express the **CD4** marker. They recognize antigens presented by MHC Class II molecules and secrete cytokines that "help" B cells produce antibodies and activate cytotoxic T cells and macrophages. 2. **Killer T cells (Cytotoxic T cells/Tc cells):** Express the **CD8** marker. They recognize antigens presented by MHC Class I molecules and directly destroy virally infected cells or tumor cells by releasing perforins and granzymes. **Why other options are incorrect:** * **A. B cells:** These are responsible for humoral immunity. They differentiate into plasma cells to produce antibodies. They do not have "helper" or "killer" subtypes. * **C. Monocytes:** These are mononuclear phagocytic leukocytes found in the blood. They are precursors to macrophages, not lymphocytes. * **D. Macrophages:** These are professional phagocytes and Antigen-Presenting Cells (APCs). While they kill pathogens via phagocytosis, they are not classified as "Killer cells" in the context of lymphocyte subsets. **NEET-PG High-Yield Pearls:** * **MHC Restriction:** CD4+ (Helper) cells are **MHC II** restricted, while CD8+ (Killer) cells are **MHC I** restricted (Rule of 8: 4×2=8 and 8×1=8). * **CD4:CD8 Ratio:** In a healthy individual, the normal ratio is approximately **2:1**. This ratio is characteristically reversed in HIV/AIDS. * **Natural Killer (NK) Cells:** Do not confuse "Killer T cells" with NK cells. NK cells are part of innate immunity and do not require prior sensitization or MHC restriction.

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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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Major Histocompatibility Complex

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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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Immunodeficiency Disorders

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Transplantation Immunology

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Tumor Immunology

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Immunology — MCQs

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