Immunology Practice Questions

Q: A 1-year-old boy is brought to the OPD with complaints of inability to gain weight and chronic diarrhea. He was growing well until 6 months of age, after which he started developing recurrent episodes of pneumonia. Family history is positive for similar symptoms in a maternal uncle. On examination, he is below the 3rd percentile for weight. Tonsils are absent. Stool is positive for Giardia. Which of the following is not true regarding his condition?

Both humoral and cell-mediated immunity are affected. **Explanation:** The clinical presentation—a male infant, onset of symptoms after 6 months (when maternal IgG wanes), recurrent pyogenic infections (pneumonia), absent tonsils, and a positive family history in a maternal uncle (X-linked inheritance)—points directly to **X-linked Agammaglobulinemia (XLA)**, also known as **Bruton’s Agammaglobulinemia**. **1. Why Option C is the correct answer (The "Not True" statement):** In XLA, the defect is specifically in **humoral immunity**. The mutation in the **Btk gene** prevents pre-B cells from maturing into B cells. However, **T-cell mediated immunity remains intact**. Patients can handle most viral and fungal infections normally, though they are susceptible to certain enteroviruses and *Giardia* (due to lack of secretory IgA). **2. Analysis of Incorrect Options:** * **Option A:** True. Since B-cell maturation is arrested, there is a profound deficiency of all classes of immunoglobulins (IgG, IgA, IgM, IgE, and IgD). * **Option B:** True. Lymph nodes in XLA lack **germinal centers and follicles**, as these areas are primarily composed of B-cells. Similarly, tonsils and Peyer's patches are atrophic or absent. * **Option D:** True. The condition is caused by a mutation in the **Bruton’s tyrosine kinase (Btk)** gene located on the X chromosome (Xq21.3-22). **Clinical Pearls for NEET-PG:** * **Classic Triad:** Male infant + Recurrent pyogenic infections after 6 months + Absent B-cells in peripheral blood. * **Common Pathogens:** *S. pneumoniae, H. influenzae* (respiratory) and *Giardia lamblia* (GI tract). * **Diagnosis:** Flow cytometry showing absent or <2% CD19+ B-cells. * **Treatment:** Intravenous Immunoglobulin (IVIG) replacement; Live vaccines are contraindicated.

Q: DiGeorge syndrome is characterized by a deficiency of which of the following?

T lymphocytes. **Explanation:** **DiGeorge Syndrome (DGS)** is a primary immunodeficiency caused by a microdeletion on chromosome **22q11.2**. The core defect lies in the failure of the **3rd and 4th pharyngeal pouches** to develop during embryogenesis. **Why T lymphocytes is the correct answer:** The thymus gland originates from the 3rd and 4th pharyngeal pouches. In DGS, **thymic hypoplasia or aplasia** occurs, leading to a failure in T-cell maturation. Since the thymus is the primary site where T-cell precursors differentiate and "learn" self-tolerance, its absence results in a profound deficiency of mature **T lymphocytes**, leading to impaired cell-mediated immunity and increased susceptibility to viral, fungal, and protozoal infections. **Why other options are incorrect:** * **A & D (B lymphocytes and Antibodies):** The development of B cells in the bone marrow is initially unaffected. While antibody production (humoral immunity) may be secondary impaired due to a lack of "T-helper" cell signals, the primary and diagnostic deficiency is cellular (T-cell) in nature. * **C (Both B and T lymphocytes):** This pattern is characteristic of **SCID (Severe Combined Immunodeficiency)**, not DiGeorge Syndrome. In DGS, the B-cell count is typically normal. **High-Yield Clinical Pearls for NEET-PG:** * **CATCH-22 Mnemonic:** **C**onotruncal cardiac defects (e.g., Tetralogy of Fallot), **A**bnormal facies, **T**hymic hypoplasia, **C**left palate, **H**ypocalcemia (due to parathyroid hypoplasia), and **22**q11 deletion. * **Chest X-ray:** Look for the **absence of a thymic shadow** in a neonate. * **Diagnosis:** Confirmed via **FISH** (Fluorescence In Situ Hybridization) for the 22q11.2 deletion. * **Hypocalcemia:** Occurs because the parathyroid glands also develop from the 3rd/4th pouches; this often presents as neonatal tetany/seizures.

Q: Which of the following activates the classical complement pathway?

Immune complex. ### Explanation The complement system is a crucial component of innate immunity consisting of three distinct pathways: Classical, Alternative, and Lectin. **1. Why "Immune Complex" is correct:** The **Classical Pathway** is primarily triggered by **Antigen-Antibody complexes (Immune complexes)**. Specifically, the C1 complex (C1q, C1r, C1s) binds to the Fc portion of **IgM** or **IgG** (subclasses IgG1, IgG2, and IgG3) that has already bound to an antigen. This binding induces a conformational change in C1q, initiating the proteolytic cascade. **2. Why the other options are incorrect:** * **Lipopolysaccharide (LPS):** Found in the outer membrane of Gram-negative bacteria, LPS is a potent activator of the **Alternative Pathway**. * **Exotoxin:** Most bacterial exotoxins do not directly activate the complement cascade; however, certain components like Teichoic acid (Gram-positive) trigger the Alternative Pathway. * **Zymosan:** This is a polysaccharide derived from **yeast cell walls** and is a classic laboratory activator of the **Alternative Pathway**. **Clinical Pearls & High-Yield Facts for NEET-PG:** * **C3:** The most abundant complement component and the common point where all three pathways converge. * **C1q:** The recognition unit for the Classical pathway. * **C-Reactive Protein (CRP):** Can also activate the Classical pathway by binding directly to C1q (independent of antibodies). * **Memory Aid:** "GM makes a Classic car" (Ig**G** and Ig**M** activate the **Classic**al pathway). * **Inhibitor:** C1 esterase inhibitor deficiency leads to **Hereditary Angioedema**.

Q: After binding of complement and antibody on the surface of encapsulated bacteria, the process of phagocytosis by polymorphonuclear leukocytes/macrophages is enhanced by all of the following opsonins, except?

CD11b/CD18. **Explanation** The core concept tested here is the distinction between **opsonins** (molecules that coat a pathogen) and **opsonin receptors** (molecules on the phagocyte that bind those coats). **Why CD11b/CD18 is the correct answer:** CD11b/CD18 (also known as **Mac-1** or Complement Receptor 3/CR3) is not an opsonin; it is an **integrin receptor** located on the surface of polymorphonuclear leukocytes (PMNs) and macrophages. It functions by binding to iC3b (an opsonin) attached to the bacteria. While it is essential for the *process* of phagocytosis and adhesion, it is a cellular receptor, not a circulating serum factor that coats the bacteria. **Analysis of incorrect options (Opsonins):** * **C3b:** This is the most potent opsonin of the complement system. It coats the bacterial surface and is recognized by the CR1 receptor on phagocytes. * **IgG:** Specifically IgG1 and IgG3 subclasses act as powerful opsonins. Their Fc portion binds to Fcγ receptors on phagocytes, significantly enhancing ingestion. * **Mannose-binding lectin (MBL):** MBL is a pattern recognition receptor that acts as a "collectin." It binds to carbohydrate patterns on encapsulated bacteria and can act directly as an opsonin or activate the lectin complement pathway. **High-Yield Clinical Pearls for NEET-PG:** * **Leukocyte Adhesion Deficiency (LAD) Type 1:** Caused by a deficiency in the β2-integrin subunit (**CD18**). Clinical features include delayed separation of the umbilical cord, recurrent bacterial infections without pus formation, and extreme leukocytosis. * **Most powerful opsonins:** IgG and C3b. * **Opsonization** neutralizes the negative surface charge (zeta potential) of encapsulated bacteria (like *S. pneumoniae*), allowing the negatively charged phagocyte to approach and ingest the pathogen.

Q: Which of the following is the most potent antigen for stimulating both humoral and cell-mediated immunity?

Proteins. The potency of an antigen depends on its chemical complexity, molecular weight, and stability. **Proteins** are the most potent immunogens because they possess high structural complexity (primary to quaternary structures) and a diverse array of epitopes. **Why Proteins are the Correct Answer:** Proteins are the only class of biomolecules capable of stimulating both **Humoral Immunity** (B-cell activation) and **Cell-Mediated Immunity** (T-cell activation) [1]. Because proteins can be processed into peptides and presented via MHC molecules to T-cells, they induce "T-dependent" responses [2]. This leads to isotype switching, high-affinity antibodies, and the formation of memory cells—the hallmarks of a robust immune response. **Analysis of Incorrect Options:** * **Adjuvants (A):** These are not antigens themselves. They are substances mixed with antigens to enhance the immune response by prolonging antigen persistence or stimulating co-stimulatory signals. * **Polysaccharides (C):** These are "T-independent" antigens. They lack the peptide components required for MHC presentation to T-cells. Consequently, they primarily stimulate B-cells to produce IgM without significant memory or cell-mediated involvement. * **Lipids (D):** These are generally poor immunogens due to his structural simplicity and flexibility. They usually only become immunogenic when conjugated to a protein carrier (acting as haptens). **High-Yield Clinical Pearls for NEET-PG:** * **Haptens:** Low molecular weight substances that are antigenic (can bind to antibodies) but not immunogenic unless attached to a carrier protein. * **Conjugate Vaccines:** By attaching a polysaccharide (like *H. influenzae* type b) to a protein carrier, we convert a T-independent response into a T-dependent one, ensuring long-term immunity in infants. * **Hierarchy of Immunogenicity:** Proteins > Polysaccharides > Lipids > Nucleic acids.

Q: In the intra-epithelial region of the intestinal mucosa, what is the predominant cell population?

T cells. **Explanation:** The intestinal mucosa is a complex immunological site divided into distinct compartments: the **intra-epithelial layer** and the **lamina propria**. **Why T cells are the correct answer:** The intra-epithelial region is primarily populated by **Intraepithelial Lymphocytes (IELs)**. Over 90% of these IELs are **T cells**. Interestingly, while most peripheral T cells are CD4+, approximately 80% of IELs are **CD8+ T cells**. These cells serve as a first line of defense, maintaining mucosal integrity and providing rapid surveillance against enteric pathogens. They often express the **γδ (gamma-delta) T-cell receptor**, which is characteristic of T cells found at mucosal surfaces. **Analysis of Incorrect Options:** * **A. B cells:** While B cells are present in the gut-associated lymphoid tissue (GALT), specifically in Peyer’s patches, they are not the predominant population within the intra-epithelial layer itself. * **C. Plasma cells:** These are the effector B cells that secrete IgA. They are the most numerous immune cells in the **lamina propria** (the layer beneath the epithelium), but not within the intra-epithelial compartment. * **D. Basophils:** These are granulocytes involved in allergic responses and parasitic infections; they are rarely found in the healthy intestinal epithelium. **High-Yield Clinical Pearls for NEET-PG:** * **CD8+ T cells** dominate the intra-epithelial layer, whereas **CD4+ T cells** dominate the lamina propria. * **Secretory IgA** is the primary antibody of the mucosal immune system, produced by plasma cells in the lamina propria. * **M cells (Microfold cells)** are specialized cells in the follicle-associated epithelium that sample antigens from the intestinal lumen and deliver them to underlying lymphoid tissue. * An increase in the number of Intraepithelial Lymphocytes (IELs) is a classic histological hallmark of **Celiac Disease**.

Q: Lysosomes are thought to play an important role in which of the following processes?

Class II MHC-restricted antigen presentation. **Explanation:** The processing and presentation of antigens are divided into two distinct pathways based on the origin of the antigen and the type of MHC molecule involved. **Why Option B is correct:** **Class II MHC-restricted antigen presentation** involves the **exogenous pathway**. Extracellular pathogens (like bacteria) are internalized via endocytosis or phagocytosis into vesicles. These vesicles fuse with **lysosomes**, forming phagolysosomes. Within these acidic environments, lysosomal enzymes degrade the protein into smaller peptides. Simultaneously, Class II MHC molecules synthesized in the ER travel to these vesicles. The peptide is loaded onto the MHC II molecule (after the CLIP protein is removed) and transported to the cell surface for presentation to **CD4+ T helper cells**. **Why other options are incorrect:** * **Option A:** Class I MHC presentation involves the **endogenous pathway**. Proteins (viral or tumor antigens) are degraded in the cytoplasm by **proteasomes**, not lysosomes. The peptides are then transported into the ER via TAP transporters. * **Options C & D:** Immunoglobulin and T-cell receptor (TCR) gene rearrangements occur in the **nucleus** of B and T cells, respectively, involving RAG-1 and RAG-2 enzymes. Lysosomes play no role in genetic recombination. **High-Yield Clinical Pearls for NEET-PG:** * **MHC I** = Endogenous antigens + Proteasome + CD8+ T cells ("Rule of 8": 1 × 8 = 8). * **MHC II** = Exogenous antigens + **Lysosome** + CD4+ T cells ("Rule of 8": 2 × 4 = 8). * **Invariant Chain (Ii):** Prevents premature binding of endogenous peptides to MHC II in the ER. * **CLIP:** The remnant of the invariant chain that stays in the MHC II groove until it is exchanged for an exogenous peptide in the lysosome.

Q: Which immunoglobulin is inactive at high temperatures?

IgE. **Explanation:** The correct answer is **IgE**. This immunoglobulin is uniquely characterized by its **heat-lability**. When exposed to a temperature of **56°C for 30 to 60 minutes**, IgE undergoes denaturation and loses its ability to bind to mast cells and basophils (the Prausnitz-Küstner reaction becomes negative). This property is due to the specific structure of its Fc region, which is more sensitive to thermal stress than other antibodies. **Analysis of Options:** * **IgG (Option A):** The most abundant and stable immunoglobulin. It is heat-stable and can withstand 56°C without losing its biological activity or structural integrity. * **IgA (Option B):** Found primarily in secretions (tears, saliva, colostrum). It is relatively stable and does not lose its functional capacity at high temperatures compared to IgE. * **IgM (Option C):** The largest (pentameric) antibody and the first to appear in response to an antigen. While large, it remains heat-stable at standard laboratory inactivation temperatures (56°C). **NEET-PG High-Yield Pearls:** * **Heat Lability:** IgE is the only immunoglobulin inactivated at 56°C in 30 minutes. * **Structure:** IgE has 4 constant domains ($C_H1$ to $C_H4$) and lacks a hinge region, similar to IgM. * **Receptors:** It binds to high-affinity **FcεRI** receptors on mast cells and basophils, mediating Type I Hypersensitivity. * **Clinical Significance:** Elevated in parasitic infections (helminths) and atopic conditions (asthma, eczema). * **Prausnitz-Küstner (PK) Reaction:** A historical test for IgE-mediated hypersensitivity; heating the serum before injection abolishes the PK reaction.

Q: Which of the following features is NOT shared between T cells and B cells?

Positive selection during development. ### Explanation The correct answer is **A. Positive selection during development**. **1. Why Positive Selection is the Correct Answer:** While both T and B cells undergo **negative selection** (deletion of self-reactive cells to ensure self-tolerance), **positive selection** is a process unique to **T cell development** in the thymus. During positive selection, T cells must demonstrate the ability to bind to self-MHC molecules with moderate affinity. If they cannot recognize the host's MHC, they undergo apoptosis. B cells, which develop in the bone marrow, do not require MHC recognition to function; therefore, they do not undergo positive selection. **2. Analysis of Incorrect Options:** * **B. Class I MHC expression:** This is a shared feature. All nucleated cells in the human body express MHC Class I molecules. Since both T and B cells are nucleated lymphocytes, they both express MHC I. * **C. Antigen-specific receptors:** This is a shared feature. Both cell types are part of the adaptive immune system and possess unique surface receptors—the **T-Cell Receptor (TCR)** and the **B-Cell Receptor (BCR/Surface Ig)**—generated through V(D)J recombination to recognize specific antigens. **3. NEET-PG High-Yield Pearls:** * **Site of Maturation:** T cells mature in the **Thymus**; B cells mature in the **Bone Marrow** (or Bursa of Fabricius in birds). * **Selection Process:** * **T cells:** Undergo both Positive selection (Cortex) and Negative selection (Medulla). * **B cells:** Undergo Negative selection only. * **MHC Restriction:** T cells are "MHC restricted" (CD4 to MHC II, CD8 to MHC I), whereas B cells can recognize free, soluble antigens directly. * **Clonal Deletion:** This is the primary mechanism of central tolerance for both cell types.

Q: Which of the following is an example of Type I hypersensitivity?

Casoni's test. **Explanation:** **Type I Hypersensitivity** (Immediate/Anaphylactic) is mediated by **IgE antibodies** binding to mast cells and basophils, leading to the release of vasoactive amines like histamine upon re-exposure to an antigen. **Why Casoni’s Test is correct:** Casoni’s test is an immediate hypersensitivity skin test used for the diagnosis of **Hydatid disease** (*Echinococcus granulosus*). When a small amount of sterile hydatid fluid is injected intradermally, a wheal-and-flare response occurs within 20 minutes in sensitized individuals. This rapid reaction is a classic clinical example of a Type I hypersensitivity response. **Analysis of Incorrect Options:** * **A & B. Lepromin and Tuberculin tests:** These are examples of **Type IV (Delayed-type) hypersensitivity**. They are mediated by T-cells (not antibodies) and take 48–72 hours to manifest as induration at the injection site. * **D. Arthus reaction:** This is a localized **Type III hypersensitivity** reaction. It involves the formation of antigen-antibody (immune) complexes that deposit in local blood vessels, leading to complement activation and inflammatory tissue damage. **High-Yield Clinical Pearls for NEET-PG:** * **Type I mnemonic:** "Atopy/Anaphylaxis" (IgE). Examples: Asthma, Urticaria, Allergic rhinitis, and Casoni’s test. * **Type II:** Cytotoxic (IgG/IgM). Examples: Rh incompatibility, Myasthenia Gravis, Goodpasture syndrome. * **Type III:** Immune-Complex. Examples: SLE, Post-streptococcal glomerulonephritis (PSGN), Serum sickness. * **Type IV:** Delayed. Examples: Contact dermatitis, Graft rejection, Mantoux test. * **Note:** Casoni’s test is now largely replaced by serology (ELISA) and imaging due to low specificity and risk of sensitization.

Question 1

A 1-year-old boy is brought to the OPD with complaints of inability to gain weight and chronic diarrhea. He was growing well until 6 months of age, after which he started developing recurrent episodes of pneumonia. Family history is positive for similar symptoms in a maternal uncle. On examination, he is below the 3rd percentile for weight. Tonsils are absent. Stool is positive for Giardia. Which of the following is not true regarding his condition?

Accepted Answer

Both humoral and cell-mediated immunity are affected

Answer

All classes of immunoglobulin levels are reduced

Answer

Lymph node biopsy shows depletion of follicles

Answer

It is caused by a mutation of the Bruton's tyrosine kinase (Btk) gene

Question 2

DiGeorge syndrome is characterized by a deficiency of which of the following?

Accepted Answer

T lymphocytes

Answer

B lymphocytes

Answer

Both B and T lymphocytes

Answer

Antibodies

Question 3

Which of the following activates the classical complement pathway?

Accepted Answer

Immune complex

Answer

Lipopolysaccharide

Answer

Exotoxin

Answer

Zymosan

Question 4

After binding of complement and antibody on the surface of encapsulated bacteria, the process of phagocytosis by polymorphonuclear leukocytes/macrophages is enhanced by all of the following opsonins, except?

Accepted Answer

CD11b/CD18

Answer

C3b complement protein

Answer

IgG antibody

Answer

Mannose binding lectin (MBL)

Question 5

Which of the following is the most potent antigen for stimulating both humoral and cell-mediated immunity?

Accepted Answer

Proteins

Answer

Adjuvant

Answer

Polysaccharides

Answer

Lipids

Question 6

In the intra-epithelial region of the intestinal mucosa, what is the predominant cell population?

Accepted Answer

T cells

Answer

B cells

Answer

Plasma cells

Answer

Basophils

Question 7

Lysosomes are thought to play an important role in which of the following processes?

Accepted Answer

Class II MHC-restricted antigen presentation

Answer

Class I MHC-restricted antigen presentation

Answer

Immunoglobulin gene rearrangement

Answer

T cell receptor alpha chain rearrangement

Question 8

Which immunoglobulin is inactive at high temperatures?

Accepted Answer

IgE

Answer

IgG

Answer

IgA

Answer

IgM

Question 9

Which of the following features is NOT shared between T cells and B cells?

Accepted Answer

Positive selection during development

Answer

Class I MHC expression

Answer

Antigen-specific receptors

Answer

All of the above

Question 10

Which of the following is an example of Type I hypersensitivity?

Accepted Answer

Casoni's test

Answer

Lepromin test

Answer

Tuberculin test

Answer

Arthus reaction

Immunology — MCQs

Immunology — MCQs

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