Immunology Practice Questions

Q: What is the chemical nature of complement?

Protein. **Explanation:** The complement system is a vital component of the innate immune system, consisting of a complex network of over 30 circulating and membrane-bound proteins. **Why Protein is the Correct Answer:** Complements are primarily **globular proteins and glycoproteins** synthesized mainly by the liver (hepatocytes), though macrophages and intestinal epithelial cells also contribute. They circulate in the blood as inactive precursors (zymogens). Upon activation by specific triggers (like antigen-antibody complexes or microbial surfaces), they undergo a proteolytic cascade—where one protein cleaves the next—leading to opsonization, inflammation, and the formation of the Membrane Attack Complex (MAC). **Why Other Options are Incorrect:** * **Lipids:** Lipids serve as structural components of cell membranes or signaling molecules (e.g., prostaglandins), but they do not possess the enzymatic or cascading properties required for the complement system. * **Polysaccharides:** These are complex carbohydrates. While many complement proteins are *glycosylated* (making them glycoproteins), their functional backbone and enzymatic activity are derived from their amino acid sequences (proteins). * **Lipopolysaccharides (LPS):** LPS is a component of the Gram-negative bacterial cell wall (endotoxin). It is an **activator** of the Alternative Complement Pathway, not the chemical nature of the complement proteins themselves. **High-Yield Clinical Pearls for NEET-PG:** * **Heat Lability:** Complement is **heat-labile**; it is inactivated by heating serum at **56°C for 30 minutes**. * **Most Abundant:** **C3** is the most abundant complement protein in the serum. * **C3b:** Acts as a powerful **opsonin** (facilitates phagocytosis). * **Anaphylatoxins:** **C3a, C4a, and C5a** (with C5a being the most potent) trigger histamine release. * **MAC:** Formed by components **C5b-C9**, it leads to osmotic lysis of target cells.

Q: Which surface marker is characteristically present on Natural Killer (NK) cells?

CD 16. **Explanation:** **Natural Killer (NK) cells** are large granular lymphocytes that form a crucial part of the innate immune system. They are characteristically identified by the presence of **CD16** and **CD56**, while notably lacking the T-cell receptor (CD3). **Why CD16 is the Correct Answer:** CD16 is the **FcγRIII** (low-affinity receptor for the Fc portion of IgG). Its presence on NK cells is functional: it allows these cells to bind to antibody-coated target cells, triggering **Antibody-Dependent Cellular Cytotoxicity (ADCC)**. This is a high-yield mechanism where NK cells release perforins and granzymes to destroy virally infected or tumor cells. **Analysis of Incorrect Options:** * **CD44:** A cell-surface glycoprotein involved in cell-cell interactions, cell adhesion, and migration (notably a receptor for hyaluronic acid). It is not a specific marker for NK cells. * **CD54 (ICAM-1):** An intercellular adhesion molecule expressed on endothelial cells and immune cells. It binds to LFA-1 and is involved in leukocyte extravasation during inflammation. * **CD32 (FcγRII):** An Fc receptor found primarily on B cells, macrophages, and neutrophils. It acts as an inhibitory receptor on B cells to regulate antibody production. **High-Yield Clinical Pearls for NEET-PG:** * **NK Cell Markers:** CD16 (ADCC) and CD56 (NCAM - Neural Cell Adhesion Molecule). * **Defining Feature:** NK cells are **CD3 negative**. If a cell is CD3+ and CD56+, it is an NKT cell. * **Function:** They provide the first line of defense against intracellular pathogens and tumors by recognizing the **absence of MHC Class I** molecules (the "Missing Self" hypothesis). * **Cytokine Activation:** NK cell activity is significantly enhanced by **IL-2 and IL-12**.

Q: What is the transition mutation of GATCCT?

GGTCCT. ### Explanation **Underlying Concept: Point Mutations** Point mutations involve the substitution of a single nucleotide base. These are classified into two types: 1. **Transitions:** Replacement of a Purine by another Purine (A ↔ G) or a Pyrimidine by another Pyrimidine (C ↔ T). 2. **Transversions:** Replacement of a Purine by a Pyrimidine or vice versa (e.g., A ↔ C, G ↔ T). **Why Option A is Correct:** The original sequence is **GATCCT**. In Option A (**GGTCCT**), the second base **A** (Purine) is replaced by **G** (Purine). Since a purine is replaced by another purine, this is a **transition mutation**. **Analysis of Incorrect Options:** * **B. GTTCCT:** The second base **A** (Purine) is replaced by **T** (Pyrimidine). This is a **transversion**. * **C. GTCCCT:** The second base **A** (Purine) is replaced by **T** (transversion) AND the fourth base **C** is replaced by **C** (no change). This does not fit the single transition criteria. * **D. GGUGGT:** This sequence contains **U** (Uracil), which is found in RNA, not DNA. Furthermore, it involves multiple base changes. **High-Yield Clinical Pearls for NEET-PG:** * **Frequency:** Although there are twice as many possible transversions as transitions, **transitions** occur more frequently in the genome (approx. 2:1 ratio) because they are less likely to result in amino acid substitutions. * **Deamination:** The most common cause of transition mutations in humans is the spontaneous deamination of **5-methylcytosine to Thymine**. * **Silent Mutations:** Transitions at the third position of a codon (wobble position) often result in silent mutations, maintaining the same amino acid. * **Sickle Cell Anemia:** A classic example of a **transversion** (GAG → GTG; Glutamate to Valine).

Q: Which interleukin is secreted by macrophages and stimulates lymphocytes?

IL-1. **Explanation:** **Interleukin-1 (IL-1)** is a pro-inflammatory cytokine primarily secreted by activated **macrophages** and monocytes. Its primary role in the immune response is to act as a costimulator for T-lymphocyte activation. It promotes the proliferation of helper T-cells and enhances the maturation and clonal expansion of B-cells, effectively bridging the innate and adaptive immune systems. **Analysis of Options:** * **IL-1 (Correct):** Known as the "endogenous pyrogen," it acts on the hypothalamus to induce fever and stimulates lymphocytes to produce IL-2 and express IL-2 receptors. * **IFN-alpha:** Produced by leukocytes (mainly plasmacytoid dendritic cells) in response to viral infections. Its primary role is antiviral state induction, not lymphocyte stimulation. * **TNF-alpha:** While also secreted by macrophages, its primary role is mediating systemic inflammation, activating endothelial cells, and inducing apoptosis in tumor cells. It is a key mediator of septic shock. * **IL-6:** Secreted by macrophages and T-cells; it primarily stimulates the liver to produce **acute-phase reactants** (like CRP) and promotes B-cell differentiation into plasma cells, but it is not the primary "lymphocyte stimulator" in the context of initial activation. **High-Yield Clinical Pearls for NEET-PG:** * **The "Hot T-Bone Steak" Mnemonic:** * **IL-1:** **Hot** (Fever) * **IL-2:** Stimulates **T**-cells * **IL-3:** Stimulates **Bone** marrow (stem cells) * **IL-4:** Ig**E** production * **IL-5:** Ig**A** production & Eosinophils * **IL-1 & IL-6** are the chief mediators of the **Acute Phase Response**. * **IL-8** is the major chemotactic factor for **Neutrophils** ("Clean up on aisle 8").

Q: A 35-year-old male patient presents with numerous subcutaneous hemorrhages. History and physical examination reveal that he has been taking sedormid (a sedative) for the past week. Laboratory tests indicate normal hemoglobin and white blood cell levels with significant thrombocytopenia. You suspect that he has developed a drug-induced type II hypersensitivity reaction. This reaction may occur if the drug acts as which of the following?

Acts as a hapten. **Explanation** The clinical presentation of subcutaneous hemorrhages (purpura) and isolated thrombocytopenia following drug intake (Sedormid) is a classic example of **Drug-Induced Immune Thrombocytopenia**, a **Type II Hypersensitivity reaction**. **Why Option B is Correct:** Drugs like Sedormid, penicillin, or quinidine are small molecules (low molecular weight) that are not immunogenic on their own. They act as **haptens**. In this specific reaction, the drug binds to the surface of platelets (the carrier protein). This drug-platelet complex becomes immunogenic, stimulating the production of antibodies (IgG or IgM). These antibodies bind to the drug-coated platelets, leading to their destruction via the **complement system** (classical pathway) or **opsonization** (phagocytosis by splenic macrophages), resulting in thrombocytopenia. **Why Incorrect Options are Wrong:** * **Option A:** Activation of T-cytotoxic cells is characteristic of **Type IV (Delayed) Hypersensitivity**, not Type II. * **Option C:** Mast cell degranulation and mediator release (histamine) are the hallmarks of **Type I (Immediate) Hypersensitivity**, typically seen in anaphylaxis or urticaria. * **Option D:** Respiratory burst and oxygen radical production are primary mechanisms used by neutrophils and macrophages to kill phagocytosed bacteria, not the primary mechanism of drug-induced platelet destruction. **High-Yield Clinical Pearls for NEET-PG:** * **Type II Hypersensitivity** is "Antibody-Mediated" (Cytotoxic). * **Common Examples:** Erythroblastosis fetalis, Rheumatic fever, Goodpasture syndrome, Myasthenia gravis, and Graves' disease. * **Hapten Rule:** A hapten is a substance that is **antigenic** (can react with antibodies) but not **immunogenic** (cannot elicit an immune response) unless conjugated to a carrier protein.

Q: Deficiency of C1 inhibitor results in?

Hereditary Angioneurotic Edema. **Explanation:** **C1 inhibitor (C1-INH)** is a crucial regulatory protein that inhibits the classical complement pathway by inactivating C1r and C1s. It also plays a vital role in the kinin system by inhibiting **Kallikrein** and **Factor XIIa**. 1. **Why Option B is Correct:** Deficiency of C1-INH leads to uncontrolled activation of the kinin system. This results in the excessive production of **Bradykinin**, a potent vasodilator that increases vascular permeability. Clinically, this manifests as **Hereditary Angioneurotic Edema (HANE)**, characterized by recurrent episodes of non-pitting edema of the skin, larynx (causing airway obstruction), and gastrointestinal tract (causing abdominal pain). 2. **Why Other Options are Incorrect:** * **Option A (SLE):** Deficiency of early complement components (**C1q, C1r, C1s, C2, C4**) is strongly associated with SLE-like syndromes due to the failure of immune complex clearance. * **Option C (Pyogenic Infections):** Recurrent pyogenic infections (e.g., *S. pneumoniae*) are typically seen in **C3 deficiency**, as C3 is central to opsonization and the recruitment of inflammatory cells. * **Option D (Gram-negative bacteremia):** Deficiency of the late complement components (**C5-C9**, the Membrane Attack Complex) predisposes individuals specifically to *Neisseria* infections (meningitis and gonorrhea). **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Screen with **C4 levels** (consistently low in HANE). Confirm with C1-INH functional/quantitative assays. * **Treatment:** Acute attacks are treated with **C1-INH concentrate** or **Icatibant** (Bradykinin B2 receptor antagonist). Prophylaxis often involves attenuated androgens (e.g., **Danazol**). * **Key Distinction:** Unlike allergic angioedema, HANE does **not** present with urticaria (hives) or pruritus.

Q: Which component of bacteria stimulates innate immunity?

Carbohydrate sequences in the cell wall. ### Explanation The correct answer is **A. Carbohydrate sequences in the cell wall.** **Why it is correct:** Innate immunity relies on the recognition of **Pathogen-Associated Molecular Patterns (PAMPs)** by **Pattern Recognition Receptors (PRRs)**, such as Toll-like receptors (TLRs). Carbohydrate sequences in the bacterial cell wall, specifically **Peptidoglycan** (found in both Gram-positive and Gram-negative bacteria) and **Lipopolysaccharide (LPS)** (found in Gram-negative bacteria), are classic PAMPs. These conserved structures are unique to microbes and are essential for their survival, making them the primary targets for immediate innate immune activation. **Why the other options are incorrect:** * **B. Flagella:** While flagellin (the protein in flagella) can stimulate innate immunity via TLR-5, the cell wall carbohydrates (LPS/Peptidoglycan) are considered the more fundamental and potent stimulators of the generalized innate response across almost all bacterial species. * **C. Bacterial cell membrane:** The phospholipid bilayer of bacteria is structurally similar to human cell membranes. Innate immunity targets unique microbial structures; therefore, the cell wall (which humans lack) is a more specific and potent trigger than the membrane. * **D. Nucleus:** Bacteria are **prokaryotes** and do not possess a membrane-bound nucleus. Their genetic material exists as a nucleoid. **High-Yield Clinical Pearls for NEET-PG:** * **TLR-4** recognizes **LPS** (Endotoxin) of Gram-negative bacteria. * **TLR-2** recognizes **Peptidoglycan** and Teichoic acid of Gram-positive bacteria. * **Mannose-binding lectin (MBL)** is a PRR that recognizes terminal mannose residues (carbohydrates) on bacterial surfaces, initiating the **Lectin pathway** of the Complement system. * **PAMPs** are germline-encoded and do not require prior exposure (unlike adaptive immunity).

Q: Which of the following cells do not typically present MHC class II molecules?

Eosinophils. **Explanation:** The core concept tested here is the distribution of **Major Histocompatibility Complex (MHC) Class II** molecules. Unlike MHC Class I, which is expressed on all nucleated cells, MHC Class II is constitutively expressed only on **Professional Antigen-Presenting Cells (pAPCs)**. These cells are essential for activating CD4+ T-helper cells. **Why Eosinophils are the Correct Answer:** Eosinophils are primarily granulocytes involved in parasitic infections and allergic responses. While they can be induced to express MHC II under specific inflammatory conditions, they are **not** considered typical or professional APCs. In the context of standard immunology and NEET-PG questions, granulocytes (Neutrophils, Eosinophils, Basophils) are categorized as cells that do not typically present MHC II. **Analysis of Incorrect Options:** * **Dendritic Cells:** These are the most potent professional APCs. They are the only cells capable of activating naive T-cells. * **Macrophages:** These are professional APCs that present phagocytosed antigens to effector T-cells at the site of infection. * **Lymphocytes (specifically B-cells):** B-lymphocytes are professional APCs. They internalize antigens via surface immunoglobulins and present them to T-helper cells to receive signals for isotype switching and memory cell formation. **High-Yield Clinical Pearls for NEET-PG:** * **MHC II Distribution:** Professional APCs = **B**-cells, **D**endritic cells, and **M**acrophages (Mnemonic: **BDM**). * **MHC Restriction:** MHC Class I interacts with **CD8+** T-cells (1 × 8 = 8), while MHC Class II interacts with **CD4+** T-cells (2 × 4 = 8). * **Non-Professional APCs:** Under the influence of **IFN-gamma**, certain non-professional cells (like vascular endothelial cells or thyroid epithelial cells) can transiently express MHC II.

Q: Transfusion reactions and erythroblastosis fetalis are examples of which type of hypersensitivity reaction?

Type II hypersensitivity. **Explanation:** **Type II Hypersensitivity (Cytotoxic)** is the correct answer. This reaction is mediated by **IgG or IgM antibodies** directed against antigens present on the surface of specific cells or tissues. When these antibodies bind to the cell surface (e.g., Red Blood Cells), they activate the complement system or lead to Antibody-Dependent Cellular Cytotoxicity (ADCC), resulting in cell lysis or phagocytosis. * In **Transfusion Reactions**, host antibodies attack donor RBC antigens (ABO incompatibility). * In **Erythroblastosis Fetalis**, maternal Rh antibodies cross the placenta and destroy fetal Rh+ RBCs. **Why other options are incorrect:** * **Type I (Immediate):** Mediated by **IgE** and mast cell degranulation (e.g., Anaphylaxis, Asthma). * **Type III (Immune-complex):** Caused by deposition of **antigen-antibody complexes** in tissues, leading to inflammation (e.g., SLE, Post-streptococcal glomerulonephritis). * **Type IV (Delayed):** A **cell-mediated** response involving T-lymphocytes, not antibodies (e.g., Mantoux test, Contact dermatitis). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Types:** **ACID** (**A**naphylactic, **C**ytotoxic, **I**mmune-complex, **D**elayed). * **Type II Examples:** Goodpasture syndrome, Myasthenia gravis, Rheumatic fever, and Pemphigus vulgaris. * **Coombs Test:** Used specifically to detect Type II reactions in immunohematology. * **Drug-induced Hemolytic Anemia** is also a classic Type II reaction.

Question 1

What is the chemical nature of complement?

Accepted Answer

Protein

Answer

Lipid

Answer

Polysaccharide

Answer

Lipo polysaccharide

Question 2

Which surface marker is characteristically present on Natural Killer (NK) cells?

Accepted Answer

CD 16

Answer

CD 44

Answer

CD 54

Answer

CD 32

Question 3

What is the transition mutation of GATCCT?

Accepted Answer

GGTCCT

Answer

GTTCCT

Answer

GTCCCT

Answer

GGUGGT

Question 4

Which interleukin is secreted by macrophages and stimulates lymphocytes?

Accepted Answer

IL-1

Answer

IFN alpha

Answer

TNF alpha

Answer

IL-6

Question 5

A 35-year-old male patient presents with numerous subcutaneous hemorrhages. History and physical examination reveal that he has been taking sedormid (a sedative) for the past week. Laboratory tests indicate normal hemoglobin and white blood cell levels with significant thrombocytopenia. You suspect that he has developed a drug-induced type II hypersensitivity reaction. This reaction may occur if the drug acts as which of the following?

Accepted Answer

Acts as a hapten

Answer

Activates T cytotoxic cells

Answer

Induces mast cell degranulation, releasing mediators such as histamine, leukotrienes, and prostaglandins

Answer

Induces oxygen radical production through the respiratory burst pathway

Question 6

Deficiency of C1 inhibitor results in?

Accepted Answer

Hereditary Angioneurotic Edema

Answer

Systemic Lupus Erythematosus (SLE)

Answer

Severe recurrent pyogenic infections

Answer

Gram-negative bacteremia

Question 7

Which component of bacteria stimulates innate immunity?

Accepted Answer

Carbohydrate sequences in the cell wall

Answer

Flagella

Answer

Bacterial cell membrane

Answer

Nucleus

Question 8

Which of the following cells do not typically present MHC class II molecules?

Accepted Answer

Eosinophils

Answer

Macrophage

Answer

Dendritic cells

Answer

Lymphocytes

Question 9

Transfusion reactions and erythroblastosis fetalis are examples of which type of hypersensitivity reaction?

Accepted Answer

Type II hypersensitivity

Answer

Type I hypersensitivity

Answer

Type III hypersensitivity

Answer

Type IV hypersensitivity

Question 10

The Ouchterlony procedure is a type of immunodiffusion characterized by which of the following?

Accepted Answer

Double diffusion in two dimensions

Answer

Single diffusion in one dimension

Answer

Double diffusion in one dimension

Answer

Single diffusion in two dimensions

Immunology — MCQs

Immunology — MCQs

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