Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 201: All of the following are a part of innate immunity except?

A. Complement
B. NK cells
C. Macrophages
D. T cells (Correct Answer)

Explanation: **Explanation:** The immune system is broadly divided into **Innate Immunity** (non-specific, immediate response) and **Acquired/Adaptive Immunity** (specific, delayed response with memory). **Why T cells are the correct answer:** T cells (T lymphocytes) are the hallmark of **Adaptive Immunity**. They possess highly specific receptors (TCRs) generated through genetic rearrangement to recognize specific antigens. They provide cell-mediated immunity and develop "memory," allowing for a faster and more potent response upon re-exposure. Therefore, they are not part of the innate system. **Analysis of Incorrect Options:** * **Complement (A):** These are plasma proteins that act as a chemical barrier. They are activated immediately upon pathogen entry via the alternative or lectin pathways, making them a crucial humoral component of innate immunity. * **NK cells (B):** Natural Killer cells are large granular lymphocytes that provide the first line of defense against virally infected cells and tumors. Unlike T cells, they lack antigen-specific receptors and do not require prior sensitization. * **Macrophages (C):** These are professional phagocytes derived from monocytes. They act as cellular components of innate immunity by engulfing pathogens via non-specific pattern recognition receptors (PRRs). **High-Yield Clinical Pearls for NEET-PG:** * **Innate Immunity Components:** Physical barriers (Skin/Mucosa), Chemical barriers (Complement/Lysozyme), and Cellular components (Neutrophils, Macrophages, NK cells, Dendritic cells). * **Bridge between systems:** Dendritic cells and Macrophages act as a bridge by functioning as Antigen Presenting Cells (APCs) to activate the adaptive system. * **NK Cell Marker:** CD56 is the characteristic marker for NK cells. * **Specificity:** Innate immunity recognizes **PAMPs** (Pathogen-Associated Molecular Patterns) via **PRRs** (like Toll-like Receptors).

Question 202: HLA-A, B, and C genes belong to which class of the HLA complex located on the 6th chromosome?

A. Class I (Correct Answer)
B. Class II
C. Class III
D. Class IV

Explanation: **Explanation:** The **Human Leukocyte Antigen (HLA)** system is the human version of the Major Histocompatibility Complex (MHC), located on the **short arm of Chromosome 6**. It is divided into three distinct classes based on structure and function. **1. Why Class I is Correct:** HLA Class I molecules are encoded by three highly polymorphic gene loci: **HLA-A, HLA-B, and HLA-C**. These molecules are expressed on the surface of almost all **nucleated cells** and platelets. Their primary role is to present endogenous antigens (like viral or tumor proteins) to **CD8+ Cytotoxic T-cells**. **2. Why other options are incorrect:** * **Class II:** These are encoded by the **HLA-D** region (specifically HLA-DR, DQ, and DP). Unlike Class I, they are expressed only on **Antigen-Presenting Cells (APCs)** like macrophages, B-cells, and dendritic cells, and they present exogenous antigens to **CD4+ Helper T-cells**. * **Class III:** These genes are located between Class I and II regions. They do not encode antigen-presenting molecules but instead code for components of the **complement system** (C2, C4) and inflammatory cytokines like **TNF-alpha**. * **Class IV:** This is not a standard classification used in the HLA system. **High-Yield Clinical Pearls for NEET-PG:** * **Rule of 8:** MHC I × CD8 = 8; MHC II × CD4 = 8. * **Structure:** Class I consists of one heavy chain and a **$\beta_2$-microglobulin** (encoded on Chromosome 15). Class II consists of two heavy chains ($\alpha$ and $\beta$). * **Key Disease Associations:** * **HLA-B27:** Ankylosing spondylitis, Reiter’s syndrome. * **HLA-DR3/DR4:** Type 1 Diabetes Mellitus. * **HLA-DQ2/DQ8:** Celiac disease.

Question 203: What is the mechanism of action of a superantigen?

A. Binds to B7 and CD28 costimulatory molecules.
B. Binds to the beta chain of the T cell receptor and MHC class II molecules of antigen-presenting cells, stimulating T cell activation. (Correct Answer)
C. Binds to the CD4+ molecule, causing T cell activation.
D. Is presented by macrophages to a larger-than-normal number of T helper CD4+ lymphocytes.

Explanation: ### Explanation **Mechanism of Superantigens** Superantigens (SAgs) are potent immunostimulatory molecules (mostly bacterial toxins) that bypass the standard antigen-processing pathway. Unlike conventional antigens, which are processed into peptides and presented within the MHC groove, superantigens bind **externally** to the **Vβ (variable beta) chain** of the T-cell receptor (TCR) and the **MHC class II** molecule on Antigen-Presenting Cells (APCs). This "molecular bridge" results in the non-specific activation of up to 20% of the body’s T-cell population, leading to a massive release of cytokines (Cytokine Storm), primarily TNF-α, IL-1, and IL-2. **Analysis of Options:** * **Option A:** B7 (on APCs) and CD28 (on T-cells) are standard costimulatory molecules. While they are involved in normal T-cell activation, they are not the primary binding targets of superantigens. * **Option C:** Superantigens do not bind directly to the CD4 molecule; they bind to the Vβ region of the TCR. * **Option D:** This is the key distinction. Conventional antigens are **processed and presented** by macrophages to a specific few T-cells (0.001%). Superantigens are **not processed**; they bind directly to the outside of the MHC-II/TCR complex. **High-Yield Clinical Pearls for NEET-PG:** * **Examples of Superantigens:** * *Staphylococcus aureus:* TSST-1 (Toxic Shock Syndrome Toxin) and Enterotoxins (Food poisoning). * *Streptococcus pyogenes:* SpeA and SpeC (Pyrogenic exotoxins causing Scarlet fever/STSS). * **Key Consequence:** Massive release of **IFN-γ and IL-2** (from T-cells) and **TNF-α and IL-1** (from macrophages), leading to shock and multi-organ failure. * **Mnemonic:** Superantigens bind **MHC-II** (not MHC-I) and the **Vβ chain** (not Vα).

Question 204: Anaphylactic shock is caused by which type of hypersensitivity reaction?

A. Type II
B. Type III
C. Type IV
D. Type I (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Type I Hypersensitivity** **Mechanism:** Type I hypersensitivity, also known as **Immediate Hypersensitivity**, is mediated by **IgE antibodies**. Upon initial exposure to an allergen (e.g., penicillin, bee sting, peanuts), IgE is produced and binds to the surface of **mast cells and basophils** via Fc receptors. On re-exposure, the allergen cross-links these IgE molecules, triggering degranulation and the release of potent inflammatory mediators like **histamine**, leukotrienes, and prostaglandins. This leads to systemic vasodilation and bronchoconstriction, resulting in **Anaphylactic Shock**. **Why other options are incorrect:** * **Type II (Cytotoxic):** Mediated by **IgG or IgM** antibodies directed against antigens on specific cell surfaces or tissues (e.g., ABO incompatibility, Myasthenia Gravis). * **Type III (Immune-complex):** Caused by the deposition of **antigen-antibody complexes** in tissues, leading to complement activation and neutrophil recruitment (e.g., SLE, Serum Sickness, Arthus reaction). * **Type IV (Delayed-type):** This is **cell-mediated** (T-cells), not antibody-mediated. It takes 48–72 hours to manifest (e.g., Mantoux test, Contact dermatitis). **High-Yield Clinical Pearls for NEET-PG:** * **Drug of choice for Anaphylaxis:** Adrenaline (Epinephrine) 1:1000 given **Intramuscularly (IM)**. * **Marker for Mast Cell activation:** Serum **Tryptase** levels (measured post-reaction). * **Coombs and Gell Classification:** The standard classification system for these four types of hypersensitivity. * **Atopy:** A genetic predisposition to develop Type I reactions (allergic rhinitis, asthma, eczema).

Question 205: What part of an antibody is related to the antigen idiotype?

A. Fc fragment
B. Hinge region
C. C-terminal
D. N-terminal (Correct Answer)

Explanation: **Explanation:** The **idiotype** of an antibody refers to the unique set of antigenic determinants (idiotopes) located within the **Variable (V) regions** of the heavy and light chains. These regions form the **antigen-binding site (paratope)**. 1. **Why N-terminal is correct:** The polypeptide chains of an antibody have a polarity. The **N-terminal** (amino-terminal) ends of both the heavy and light chains contain the variable domains ($V_H$ and $V_L$). Since the idiotype is defined by the specific amino acid sequence in these variable domains that determines antigen specificity, the N-terminal is the structural site related to the idiotype. 2. **Why other options are incorrect:** * **Fc fragment:** This is the "Fragment crystallizable" region composed only of constant domains ($C_H2, C_H3$). it mediates biological effector functions (e.g., complement fixation, opsonization) but does not bind antigens. * **Hinge region:** This is a flexible amino acid stretch between the $C_H1$ and $C_H2$ domains that allows the two Fab arms to move; it does not determine idiotype. * **C-terminal:** The Carboxy-terminal ends of the heavy chains are located within the Fc region. They are constant for a given isotype and do not contribute to the unique antigen-binding idiotype. **High-Yield Clinical Pearls for NEET-PG:** * **Isotype:** Determined by the heavy chain constant region (e.g., IgG vs. IgA). * **Allotype:** Allelic variations in constant regions between individuals of the same species. * **Idiotype:** Unique to a specific antibody molecule produced by a single B-cell clone; anti-idiotypic antibodies are used in some therapeutic regulations. * **Papain digestion** cleaves *above* the hinge region to produce 2 Fab and 1 Fc fragment, while **Pepsin** cleaves *below* the hinge to produce one $F(ab')_2$ fragment.

Question 206: Natural killer (NK) cells provide immunity against which of the following?

A. Viruses (Correct Answer)
B. Bacteria
C. Fungi
D. Chlamydia

Explanation: **Explanation:** **Natural Killer (NK) cells** are a type of cytotoxic lymphocyte critical to the **innate immune system**. They play a major role in the rejection of **virally infected cells** and tumor cells. **Why Viruses is the correct answer:** NK cells function by identifying cells that lack or have "downregulated" **MHC Class I molecules**. Many viruses (such as CMV and HIV) attempt to evade the immune system by inhibiting MHC Class I expression to avoid detection by CD8+ T-cells. NK cells utilize the **"Missing Self" hypothesis**: when their inhibitory receptors do not find MHC Class I on a host cell, they release **perforins and granzymes**, inducing apoptosis in the infected cell. This provides a rapid response before the adaptive immune system is fully activated. **Why other options are incorrect:** * **Bacteria & Fungi:** Immunity against these extracellular or pyogenic pathogens primarily relies on **neutrophils, macrophages, and the complement system** (innate), as well as B-cells/antibodies (adaptive). * **Chlamydia:** While Chlamydia is an intracellular bacterium, the primary defense involves **Th1-mediated responses** and interferon-gamma (IFN-γ) activation of macrophages, rather than direct NK cell-mediated lysis. **NEET-PG High-Yield Pearls:** * **Markers:** NK cells are identified by the presence of **CD56** and **CD16** (FcγRIII) and the **absence of CD3**. * **Antibody-Dependent Cellular Cytotoxicity (ADCC):** Through the CD16 receptor, NK cells bind to IgG-coated target cells and kill them. * **Cytokine Production:** NK cells are a major source of **IFN-γ**, which activates macrophages to kill phagocytosed microbes. * **Origin:** They are derived from the **Common Lymphoid Progenitor (CLP)** but do not require the thymus for maturation.

Question 207: Which of the following represents a delayed type of hypersensitive reaction?

A. Arthus reaction
B. Bronchial asthma
C. Hemolytic anemia
D. All of the above (Correct Answer)

Explanation: **Explanation** Hypersensitivity reactions are exaggerated immune responses that cause tissue damage. They are classified into four types (Gell and Coombs classification). While the question asks for a "delayed type" reaction, it is important to note that in many clinical scenarios, multiple hypersensitivity mechanisms overlap. 1. **Bronchial Asthma (Type I):** This is an **Immediate Hypersensitivity** reaction mediated by IgE antibodies. Upon exposure to an allergen, mast cells degranulate, releasing histamine and leukotrienes, leading to bronchospasm. 2. **Hemolytic Anemia (Type II):** This is a **Cytotoxic Hypersensitivity** reaction. Antibodies (IgG/IgM) bind to antigens on the surface of red blood cells, leading to complement activation and cell lysis. 3. **Arthus Reaction (Type III):** This is an **Immune-Complex Mediated** reaction. It occurs when local formation of antigen-antibody complexes leads to vasculitis and localized tissue necrosis. **Note on the Question Structure:** In the context of NEET-PG, this specific question is often used to test the student's ability to recognize that "delayed" can sometimes be used loosely in clinical practice to describe the **late-phase response** of Type I (Asthma) or the **evolution** of Type III (Arthus) reactions. However, strictly speaking, **Type IV** is the only true "Delayed-Type Hypersensitivity" (DTH) mediated by T-cells (e.g., Mantoux test, Contact dermatitis). *If this question appears with "All of the above" as the marked key, it implies a focus on the clinical progression of these conditions rather than the strict Gell and Coombs classification.* **High-Yield Clinical Pearls:** * **Type I:** IgE, Mast cells, Anaphylaxis (Fastest). * **Type II:** Antibody-mediated (e.g., Goodpasture syndrome, Rheumatic fever). * **Type III:** Immune complexes (e.g., SLE, Post-streptococcal glomerulonephritis). * **Type IV:** T-cell mediated; takes 48–72 hours (e.g., Lepromin test, Graft rejection).

Question 208: Which of the following are considered anti-carcinogens?

A. Carotenoids (Correct Answer)
B. Flavonoids
C. Curcumoids
D. Benzene

Explanation: **Explanation:** **Correct Answer: A. Carotenoids** **Why it is correct:** Anti-carcinogens are substances that inhibit, delay, or reverse the process of carcinogenesis (cancer formation). **Carotenoids** (such as beta-carotene, lycopene, and lutein) are potent antioxidants. They protect cells from DNA damage by neutralizing free radicals and reactive oxygen species (ROS). Furthermore, they enhance the immune system’s surveillance against tumor cells and induce phase II detoxification enzymes, making them a primary dietary anti-carcinogen. **Analysis of Incorrect Options:** * **B. Flavonoids:** While flavonoids do possess antioxidant properties, in the specific context of standard medical entrance exams and classical biochemistry, **Carotenoids** are the most recognized and frequently cited "dietary anti-carcinogens." Flavonoids are often categorized more broadly as polyphenols. * **C. Curcumoids:** Curcumin (found in turmeric) has anti-inflammatory and anti-cancer properties; however, "Curcumoids" is a less standardized term in this specific MCQ context compared to the established role of Carotenoids. * **D. Benzene:** This is a potent **carcinogen** (specifically a Group 1 carcinogen). Chronic exposure to benzene is strongly associated with the development of Acute Myeloid Leukemia (AML) by causing chromosomal damage in bone marrow. **High-Yield Clinical Pearls for NEET-PG:** * **Other Anti-carcinogens:** Vitamin C, Vitamin E, Selenium, and Isothiocyanates (found in cruciferous vegetables). * **The Beta-Carotene Paradox:** While dietary carotenoids are protective, high-dose *supplemental* beta-carotene has been shown to increase the risk of lung cancer in heavy smokers (CARET study). * **Lycopene:** A specific carotenoid found in tomatoes, highly associated with a reduced risk of **Prostate Cancer**. * **Aflatoxin B1:** A potent carcinogen (from *Aspergillus flavus*) associated with Hepatocellular Carcinoma (HCC).

Question 209: Bruton's agammaglobulinemia is due to?

A. B-cell defect (Correct Answer)
B. IgA deficiency
C. IgM deficiency
D. IgG deficiency

Explanation: **Explanation:** **Bruton’s Agammaglobulinemia** (also known as X-linked Agammaglobulinemia or XLA) is a primary immunodeficiency caused by a mutation in the **BTK gene**, which encodes for **Bruton Tyrosine Kinase**. This enzyme is essential for the maturation of pro-B cells into mature B cells. Without functional BTK, B-cell development is arrested in the bone marrow, leading to a near-total absence of circulating B cells (CD19+, CD20+) and a subsequent lack of plasma cells. Since plasma cells produce antibodies, this results in **pan-hypogammaglobulinemia** (deficiency of all immunoglobulin classes). **Analysis of Options:** * **Option A (Correct):** The fundamental defect is the failure of B-cell maturation. Without B cells, the body cannot produce any antibodies, making this a "B-cell defect." * **Options B, C, and D (Incorrect):** While IgA, IgM, and IgG levels are indeed low in Bruton’s, these are *consequences* of the underlying B-cell maturation defect. These options describe selective deficiencies, whereas Bruton’s involves a global failure of the entire B-cell lineage. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** X-linked recessive (affects male infants). * **Clinical Presentation:** Recurrent pyogenic bacterial infections (e.g., *S. pneumoniae*, *H. influenzae*) starting after 6 months of age (once maternal IgG wanes). * **Key Finding:** Absent or rudimentary tonsils and lymph nodes (due to lack of germinal centers). * **Diagnosis:** Flow cytometry showing absent B cells (CD19/20) but **normal T-cell counts**. * **Contraindication:** Live viral vaccines (e.g., OPV) are contraindicated due to the risk of paralytic poliomyelitis.

Question 210: A young child presents with a low-grade fever, coryza, sore throat, a bright red rash on his cheeks, and a less intense erythematous rash on his body. Elevated IgG and IgM antibody titers to parvovirus suggest a diagnosis of which of the following?

A. Acute Lyme disease
B. Fifth disease (Correct Answer)
C. Possible hepatitis B infection
D. Possible subacute sclerosing panencephalitis (SSPE)

Explanation: **Explanation:** The clinical presentation described—low-grade fever followed by a characteristic **"slapped-cheek"** appearance and a reticular (lace-like) body rash—is the classic manifestation of **Erythema Infectiosum**, also known as **Fifth Disease**. This condition is caused by **Parvovirus B19**, a small, non-enveloped DNA virus. The presence of elevated IgM antibodies indicates an acute infection, while IgG signifies immune response/past exposure. **Why the other options are incorrect:** * **Acute Lyme Disease:** Caused by *Borrelia burgdorferi*, it typically presents with *Erythema migrans* (a "bull’s-eye" rash), not a slapped-cheek rash, and is associated with tick bites. * **Hepatitis B Infection:** While Parvovirus B19 can cause transient aplastic crisis, it is not a cause of Hepatitis B. HBV presents with jaundice, hepatomegaly, and specific serological markers (HBsAg, anti-HBc). * **Subacute Sclerosing Panencephalitis (SSPE):** This is a rare, fatal, progressive neurological complication occurring years after a **Measles** infection, characterized by cognitive decline and myoclonus, not an acute childhood rash. **High-Yield Clinical Pearls for NEET-PG:** * **Receptor:** Parvovirus B19 binds to the **P-antigen** (globoside) on erythroid progenitor cells. * **Complications:** 1. **Aplastic Crisis:** In patients with high RBC turnover (e.g., Sickle Cell Anemia, Hereditary Spherocytosis). 2. **Hydrops Fetalis:** If a pregnant woman is infected, the virus crosses the placenta, causing severe fetal anemia and high-output cardiac failure. 3. **Arthropathy:** More common in adults (symmetrical small joint involvement). * **Diagnosis:** PCR is the most sensitive test for immunocompromised patients; serology (IgM) is used for immunocompetent individuals.

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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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Immunology — MCQs

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