Immunology Practice Questions

Q: A 10-month-old patient presents with recurrent pyogenic infections, eczema, and severe bleeding due to thrombocytopenia. The diagnosis is Wiskott-Aldrich syndrome. This immune disorder is primarily associated with a deficiency in which components of the immune system?

Deficient humoral immunity and deficient cellular immunity. **Explanation:** **Wiskott-Aldrich Syndrome (WAS)** is an X-linked recessive primary immunodeficiency caused by a mutation in the **WASP gene**, which encodes the Wiskott-Aldrich Syndrome Protein. This protein is crucial for actin cytoskeleton remodeling in hematopoietic cells. **1. Why Option D is correct:** The defect in actin polymerization impairs the ability of immune cells to migrate, interact, and signal effectively. * **Cellular Immunity:** T-cell function and numbers progressively decline (lymphopenia), leading to impaired delayed-type hypersensitivity. * **Humoral Immunity:** There is a poor antibody response to polysaccharide antigens. Characteristically, serum **IgM levels are low**, while IgA and IgE levels are often elevated (IgG is usually normal). Because both arms of the immune system are compromised, it is classified as a **combined immunodeficiency**. **2. Why other options are incorrect:** * **Options A, B, and C:** These are incorrect because WAS is not an isolated deficiency. The clinical triad of **Infections** (immunodeficiency), **Eczema**, and **Thrombocytopenia** (micro-platelets) reflects a systemic failure of both T-cell mediated and B-cell mediated (antibody) responses. **3. Clinical Pearls for NEET-PG:** * **Mnemonic (WATER):** **W**iskott-**A**ldrich, **T**hrombocytopenia, **E**czema, **R**ecurrent infections. * **Platelet Morphology:** It is the only condition featuring **small platelets** (low Mean Platelet Volume). * **Inheritance:** X-linked Recessive (affects males). * **Malignancy Risk:** Patients have a high predisposition to Non-Hodgkin Lymphoma and autoimmune diseases. * **Definitive Treatment:** Hematopoietic stem cell transplant (HSCT).

Q: Which immunoglobulins can bind complement via the classical pathway?

IgG and IgM. **Explanation:** The classical pathway of the complement system is triggered by the binding of the **C1 complex** (specifically the C1q subunit) to the **Fc portion** of an antigen-antibody complex. 1. **Why IgG and IgM are correct:** * **IgM:** It is the most potent activator of the classical pathway. Being a pentamer, a single molecule of IgM bound to an antigen provides multiple Fc binding sites, easily cross-linking C1q. * **IgG:** It can activate the pathway, but requires at least two IgG molecules in close proximity to bind C1q. Among the subclasses, the order of efficiency is **IgG3 > IgG1 > IgG2**. (Note: IgG4 does not activate complement). 2. **Why other options are incorrect:** * **IgA:** It does not activate the classical pathway. However, it can activate the **Alternative pathway** (specifically secretory IgA). * **IgD and IgE:** Neither of these immunoglobulins has the structural capacity to bind C1q or initiate the complement cascade. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Classical Pathway:** "**GM** makes **C**lassic cars" (**I**g**G**, **I**g**M** activate **C**lassical). * **Alternative Pathway:** Activated by IgA, Endotoxins (LPS), and Cobra Venom Factor. * **Lectin Pathway:** Activated by Mannose-binding lectin (MBL) binding to microbial carbohydrates. * **C3b:** Acts as an opsonin (enhances phagocytosis). * **C5a:** The most potent anaphylatoxin and chemotactic agent for neutrophils. * **Membrane Attack Complex (MAC):** Composed of C5b-C9; deficiency leads to recurrent *Neisseria* infections.

Q: What is the main function of follicular dendritic cells?

To capture and present antigens to B cells. ### Explanation **Follicular Dendritic Cells (FDCs)** are unique cells located in the germinal centers of secondary lymphoid organs (lymph nodes and spleen). Unlike classical dendritic cells, FDCs are **not derived from hematopoietic stem cells**; they are of mesenchymal origin. **1. Why Option B is Correct:** The primary role of FDCs is to capture **native (unprocessed) antigens** trapped in the form of antigen-antibody complexes (immune complexes) via Fc receptors or complement receptors (C3b/C3d). They display these antigens on their surface for long periods. This allows **B cells** to recognize the antigen via their B-cell receptors (BCR), facilitating affinity maturation and the formation of memory B cells. **2. Why Other Options are Incorrect:** * **Option A:** Classical Dendritic Cells (e.g., Langerhans cells) process antigens and present them via MHC II molecules to **T cells**. FDCs do not express MHC II and do not interact primarily with T cells in this manner. * **Option C:** FDCs are **non-phagocytic**. Their function is to preserve the antigen on the cell surface rather than internalizing and digesting it. * **Option D:** Immunoglobulins are produced by **Plasma cells**, which are the terminally differentiated forms of B cells. **3. High-Yield Clinical Pearls for NEET-PG:** * **Origin:** FDCs are of **mesenchymal origin**, whereas classical DCs are of myeloid origin. * **Location:** Exclusively found in the **B-cell rich follicles** (germinal centers). * **Iccosomes:** FDCs shed small membrane-bound vesicles coated with antigens called iccosomes, which are endocytosed by B cells. * **HIV Reservoir:** FDCs are significant reservoirs for HIV; the virus particles can persist on the surface of FDCs for years, contributing to chronic infection.

Q: Which complement component binds with the Fc portion of IgM in the classical pathway?

C1. **Explanation:** The **Classical Pathway** of the complement system is initiated by the binding of the **C1 complex** to the Fc portion of an antigen-antibody complex. 1. **Why C1 is correct:** The C1 complex (specifically the **C1q** subunit) has receptors for the **CH2 domain of IgG** and the **CH3 domain of IgM**. IgM is a pentamer, making it a highly efficient activator of the classical pathway because a single IgM molecule can provide the multiple binding sites required for C1q to attach and become activated. Once C1q binds, it activates C1r and C1s, which then proceed to cleave C4 and C2. 2. **Why other options are incorrect:** * **C4 and C2:** These are substrates for the activated C1s enzyme. C1s cleaves C4 into C4a and C4b, and C2 into C2a and C2b. They do not bind directly to the antibody. * **C3:** This is the most abundant complement protein and the point where all three pathways (Classical, Alternative, and Lectin) converge. It is cleaved by **C3 convertase** (C4b2a in the classical pathway), not by the antibody itself. **High-Yield Clinical Pearls for NEET-PG:** * **Order of activation:** C1 → C4 → C2 → C3 → C5-C9. (Note: C4 comes before C2). * **IgM vs. IgG:** IgM is the most potent activator of the classical pathway ("**M**ighty" activator). Among IgG subclasses, the order of efficiency is **IgG3 > IgG1 > IgG2**. IgG4 does not activate the classical pathway. * **Calcium Dependency:** The C1 complex (C1qrs) is stabilized by **Calcium ions**. * **C1 Esterase Inhibitor deficiency:** Leads to **Hereditary Angioedema** due to over-activation and consumption of C4 and C2.

Q: NK cells express which of the following surface markers?

CD16, CD56. **Explanation:** Natural Killer (NK) cells are large granular lymphocytes that play a critical role in the innate immune system. They are unique because they can destroy virally infected or tumor cells without prior sensitization. **Why Option B is Correct:** The definitive surface markers for identifying NK cells are **CD16** and **CD56**. * **CD16 (FcγRIII):** This is a low-affinity receptor for the Fc portion of IgG. It allows NK cells to bind to antibody-coated target cells and destroy them via **Antibody-Dependent Cellular Cytotoxicity (ADCC)**. * **CD56 (NCAM):** An adhesion molecule used as the primary marker for NK cell identification in flow cytometry. **Analysis of Incorrect Options:** * **Option A (CD15, CD55):** CD15 is a marker for **Granulocytes** (Neutrophils) and Reed-Sternberg cells. CD55 (DAF) is a complement regulatory protein found on all blood cells. * **Option C (CD16, CD57):** While CD57 can be expressed on mature NK cells, it is not as specific or universal as CD56 for diagnostic identification. * **Option D (CD21, CD66):** CD21 (CR2) is the receptor for the **Epstein-Barr Virus (EBV)** and is found on **B-cells**. CD66 is a marker for neutrophils. **High-Yield Clinical Pearls for NEET-PG:** 1. **MHC-I Rule:** NK cells kill cells that lack **MHC Class I** molecules (the "Missing Self" hypothesis). 2. **Cytokines:** NK cell activity is stimulated by **IL-2, IL-12, and IFN-α/β**. 3. **Chediak-Higashi Syndrome:** Characterized by a functional defect in NK cells, leading to recurrent infections. 4. **Markers:** NK cells are **CD3 negative** (unlike T-cells). The presence of CD3 and CD56 together indicates NKT cells.

Q: Which of the following is NOT a function of the complement system?

Antigen presentation. The complement system is a crucial component of the innate immune system consisting of plasma proteins that "complement" the ability of antibodies and phagocytic cells to clear pathogens. ### **Why Antigen Presentation is the Correct Answer** **Antigen presentation** is a function of specialized cells known as **Antigen-Presenting Cells (APCs)**, such as dendritic cells, macrophages, and B-cells. These cells process pathogens and display their peptides on **MHC molecules** to T-cells. The complement system consists of soluble proteins and does not possess the cellular machinery required to process or present antigens. ### **Analysis of Incorrect Options** * **A. Chemotaxis:** Small fragments like **C5a** (and to a lesser extent C3a and C4a) act as potent chemoattractants. C5a specifically recruits and activates neutrophils and macrophages to the site of inflammation. * **B. Opsonization:** **C3b** (and iC3b) acts as an opsonin. It coats the surface of bacteria, making them easily "recognizable" and "tasty" for phagocytes which possess CR1 receptors. * **C. Cell Lysis:** The final step of the complement cascade is the formation of the **Membrane Attack Complex (MAC)**, composed of **C5b-C9**. This complex creates pores in the lipid bilayer of pathogens, leading to osmotic lysis. ### **High-Yield Clinical Pearls for NEET-PG** * **C3b** = **B**inds Bacteria (**Opsonization**). * **C3a, C4a, C5a** = **A**naphylatoxins (trigger mast cell degranulation). * **C5a** = Neutrophil **C**hemotaxis. * **Deficiency of C1-C4:** Associated with Systemic Lupus Erythematosus (**SLE**). * **Deficiency of C5-C9:** Increases susceptibility to **Neisseria** infections. * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** Caused by a deficiency of DAF (CD55) and MIRL (CD59), which normally protect host cells from complement-mediated lysis.

Q: Which Interleukin activates eosinophils?

IL-5. ### Explanation **Correct Answer: C. IL-5** **Mechanism and Concept:** Interleukin-5 (IL-5) is a key cytokine produced primarily by **Th2 cells** and Group 2 Innate Lymphoid Cells (ILC2s). It is the most specific cytokine for eosinophil lineage. Its primary functions include: 1. **Production:** Stimulating the bone marrow to produce eosinophils (eosinopoiesis). 2. **Activation:** Enhancing the effector functions of eosinophils, such as degranulation. 3. **Recruitment:** Promoting the migration and survival of eosinophils at sites of helminthic infections and allergic inflammation. **Analysis of Incorrect Options:** * **A. IL-1:** Produced by macrophages; it is a pro-inflammatory cytokine responsible for inducing **fever** (endogenous pyrogen) and activating vascular endothelium. * **B. IL-4:** Also produced by Th2 cells, but its primary role is inducing **B-cell class switching to IgE** and promoting Th2 differentiation. While it supports the allergic response, it does not directly activate eosinophils. * **D. IL-6:** An acute-phase reactant stimulator. It triggers the liver to produce proteins like CRP and plays a role in B-cell differentiation into plasma cells. **NEET-PG High-Yield Pearls:** * **Mnemonic for Th2 Cytokines:** "IL-**4**, **5**, and **6**." * **IL-4:** Stimulates Ig**E** (4 looks like E). * **IL-5:** Stimulates **E**osinophils (5 looks like S in Eosinophil**s**). * **Clinical Correlation:** Monoclonal antibodies targeting IL-5 (e.g., **Mepolizumab**, **Reslizumab**) or its receptor (**Benralizumab**) are used in the treatment of severe eosinophilic asthma. * **Eosinophilia:** Classically seen in **N**eoplasia, **A**llergy, **A**sthma, **C**onnective tissue diseases, and **P**arasites (Mnemonic: **NAACP**).

Q: What is the most common immunoglobulin secreted by mothers in milk and colostrum?

IgA. **Explanation:** The correct answer is **IgA**. **1. Why IgA is correct:** Secretory IgA (sIgA) is the predominant immunoglobulin in human milk, accounting for approximately 90% of the total antibodies. It is specifically adapted to survive the acidic environment of the infant's gastrointestinal tract. sIgA provides "passive mucosal immunity" by coating the infant's intestinal lining, preventing the attachment and penetration of pathogens such as *E. coli*, *Vibrio cholerae*, and various viruses. This is a crucial defense mechanism while the neonate’s own immune system is still maturing. **2. Why other options are incorrect:** * **IgG:** While IgG is the most abundant antibody in maternal **serum** and the only one that crosses the placenta to provide systemic immunity, it is present in breast milk only in very small quantities. * **IgE:** This antibody is associated with Type I hypersensitivity (allergic) reactions and parasitic infections. It is found in negligible amounts in breast milk. * **IgD:** This is primarily a B-cell surface receptor found in the serum in trace amounts; it plays no significant role in neonatal mucosal defense via breast milk. **3. High-Yield Clinical Pearls for NEET-PG:** * **Colostrum vs. Mature Milk:** The concentration of IgA is highest in **colostrum** (the first milk produced) and gradually decreases as the milk matures, though it remains the dominant antibody throughout lactation. * **Enteromammary Pathway:** Maternal IgA is produced by plasma cells in the breast that have migrated from the mother's gut-associated lymphoid tissue (GALT), ensuring the milk contains antibodies against pathogens the mother has recently encountered. * **Bifidobacterium:** Breast milk also contains the "Bifidus factor," which promotes the growth of healthy *Lactobacillus bifidus*, further inhibiting pathogenic bacteria.

Q: Increased level of IgE is seen in which of the following conditions?

Atopy. **Explanation:** **Correct Answer: A. Atopy** Immunoglobulin E (IgE) is the primary mediator of **Type I Hypersensitivity reactions**. In atopic individuals, there is a genetic predisposition to produce high levels of IgE in response to common environmental allergens. This process is driven by **Th2 cells**, which secrete IL-4 and IL-13, stimulating B-cells to undergo class-switching to IgE. The IgE then binds to high-affinity receptors (FcεRI) on mast cells and basophils, leading to degranulation upon re-exposure to the allergen. **Analysis of Incorrect Options:** * **B. Lepra reaction:** Type 1 lepra reactions are Type IV hypersensitivity (cell-mediated), while Type 2 lepra reactions (Erythema Nodosum Leprosum) are Type III hypersensitivity (immune-complex mediated). Neither is characterized by primary IgE elevation. * **C & D. Cutaneous Tuberculosis / Lupus vulgaris:** Lupus vulgaris is a common form of cutaneous TB. These represent a **Type IV (Delayed-type) hypersensitivity** response to *Mycobacterium tuberculosis*, involving T-lymphocytes and macrophages (granuloma formation), not IgE. **High-Yield Clinical Pearls for NEET-PG:** * **Job Syndrome (Hyper-IgE Syndrome):** Characterized by the triad of high IgE, recurrent "cold" staphylococcal abscesses, and coarse facial features (STAT3 mutation). * **Parasitic Infections:** IgE is also significantly elevated in helminthic infections (e.g., Ascariasis, Strongyloidiasis) to facilitate eosinophil-mediated killing. * **Prausnitz-Küstner (PK) Reaction:** An older method used to demonstrate IgE-mediated passive cutaneous anaphylaxis. * **Multiple Myeloma:** IgE myeloma is the rarest subtype of plasma cell dyscrasia.

Q: What is the central component of the complement system?

C5. **Explanation:** The complement system is a biochemical cascade of the innate immune system. **C5** is considered the central component because it serves as the critical bridge between the activation pathways (Classical, Alternative, and Lectin) and the formation of the **Membrane Attack Complex (MAC)**. The cleavage of C5 by C5-convertase into C5a and C5b marks the final enzymatic step of the cascade. Once C5b is formed, it initiates the non-enzymatic assembly of C6, C7, C8, and C9 to form the MAC (C5b-9), which leads to cell lysis. **Analysis of Options:** * **C3a:** This is an anaphylatoxin released during C3 cleavage. While it mediates inflammation and chemotaxis, it is a byproduct rather than the central anchor for terminal pathway execution. * **C3b:** Often confused as the "central" molecule because it is the most abundant and acts as a potent opsonin. However, in the context of the entire cascade's progression toward cell death, C5 is the functional pivot. * **C4:** This is an early component of the Classical and Lectin pathways. It is involved in the formation of C3-convertase but does not participate in the Alternative pathway or the terminal MAC formation. **NEET-PG High-Yield Pearls:** * **Most abundant complement:** C3. * **Most potent anaphylatoxin:** C5a (C5a > C3a > C4a). * **Potent Opsonin:** C3b (facilitates phagocytosis via CR1 receptors). * **MAC Components:** C5b, C6, C7, C8, C9. * **Clinical Correlation:** Deficiency of late complement components (C5-C9) predisposes individuals to recurrent **Neisseria** infections.

Question 1

A 10-month-old patient presents with recurrent pyogenic infections, eczema, and severe bleeding due to thrombocytopenia. The diagnosis is Wiskott-Aldrich syndrome. This immune disorder is primarily associated with a deficiency in which components of the immune system?

Accepted Answer

Deficient humoral immunity and deficient cellular immunity

Answer

Normal humoral and normal cellular immunity

Answer

Normal humoral immunity and deficient cellular immunity

Answer

Deficient humoral immunity and normal cellular immunity

Question 2

Which immunoglobulins can bind complement via the classical pathway?

Accepted Answer

IgG and IgM

Answer

IgG and IgA

Answer

IgG and IgD

Answer

IgD and IgE

Question 3

What is the main function of follicular dendritic cells?

Accepted Answer

To capture and present antigens to B cells

Answer

To capture and present antigens to T cells

Answer

Phagocytic activity

Answer

To produce immunoglobulins

Question 4

Which complement component binds with the Fc portion of IgM in the classical pathway?

Accepted Answer

C1

Answer

C2

Answer

C3

Answer

C4

Question 5

NK cells express which of the following surface markers?

Accepted Answer

CD16, CD56

Answer

CD15, CD55

Answer

CD16, CD57

Answer

CD21, CD66

Question 6

Which of the following is NOT a function of the complement system?

Accepted Answer

Antigen presentation

Answer

Chemotaxis

Answer

Opsonization

Answer

Cell lysis

Question 7

Which Interleukin activates eosinophils?

Accepted Answer

IL-5

Answer

IL-1

Answer

IL-4

Answer

IL-6

Question 8

What is the most common immunoglobulin secreted by mothers in milk and colostrum?

Accepted Answer

IgA

Answer

IgG

Answer

IgE

Answer

IgD

Question 9

Increased level of IgE is seen in which of the following conditions?

Accepted Answer

Atopy

Answer

Lepra reaction

Answer

Cutaneous Tuberculosis

Answer

Lupus vulgaris

Question 10

What is the central component of the complement system?

Accepted Answer

C5

Answer

C3a

Answer

C3b

Answer

C4

Immunology — MCQs

Immunology — MCQs

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