Immunology Practice Questions

Q: The peptide binding site on Class I MHC molecules is located in which region?

The distal domain of the alpha subunit. ### Explanation **1. Why Option B is Correct:** The Class I MHC molecule is a heterodimer consisting of a heavy **$\alpha$ chain** (encoded by HLA-A, B, or C genes) and a non-covalently linked **$\beta_2$-microglobulin**. The $\alpha$ chain is folded into three domains: $\alpha_1, \alpha_2,$ and $\alpha_3$. The peptide-binding groove (cleft) is formed by the interaction of the **$\alpha_1$ and $\alpha_2$ domains**. These are the **distal domains** (farthest from the cell membrane). This groove typically accommodates short peptides of 8–10 amino acids for presentation to CD8+ T cells. **2. Why Other Options are Incorrect:** * **Option A:** The proximal domain of the $\alpha$ subunit is the **$\alpha_3$ domain**. This region is highly conserved and serves as the binding site for the **CD8 coreceptor** of T cells, not for the peptide itself. * **Option C & D:** These options describe the structure of **Class II MHC** molecules. In Class II MHC, the peptide-binding groove is formed by the interaction of two different chains (the distal $\alpha_1$ and $\beta_1$ domains). In Class I MHC, the $\beta$ subunit ($\beta_2$-microglobulin) does not participate in forming the binding cleft. **3. High-Yield Clinical Pearls for NEET-PG:** * **MHC Class I:** Present on all nucleated cells (absent on RBCs). Presents **endogenous** antigens (e.g., viral or tumor proteins) to **CD8+ Cytotoxic T cells**. * **MHC Class II:** Present only on **Antigen-Presenting Cells (APCs)** like dendritic cells, macrophages, and B cells. Presents **exogenous** antigens to **CD4+ Helper T cells**. * **Rule of 8:** MHC I × CD8 = 8; MHC II × CD4 = 8. * **$\beta_2$-microglobulin:** It is encoded on **Chromosome 15**, while the MHC gene complex is on **Chromosome 6**. It is essential for the surface expression of Class I MHC.

Q: What is the basic structure of an antibody?

Two long and two short peptide chains. **Explanation:** The basic structure of an antibody (Immunoglobulin) is a **Y-shaped** molecule composed of four polypeptide chains: **two identical heavy (long) chains** and **two identical light (short) chains**. These chains are held together by disulfide bonds, forming a monomeric unit. 1. **Why Option D is correct:** Each antibody unit consists of two heavy chains (approx. 50-70 kDa) and two light chains (approx. 25 kDa). The heavy chains determine the **class (Isotype)** of the antibody (IgG, IgM, IgA, IgD, IgE), while the light chains are either **Kappa (κ) or Lambda (λ)**. The "V" portion of the Y-shape contains the variable regions that bind to specific antigens. 2. **Why other options are incorrect:** * **Option A & B:** A single or double chain cannot form the complex functional domains (Fab and Fc) required for antigen binding and biological activity. * **Option C:** This is incorrect because **disulfide bonds** (formed by sulfur-containing amino acid Cysteine) are essential for stabilizing the inter-chain and intra-chain structure of the immunoglobulin. **High-Yield Clinical Pearls for NEET-PG:** * **Fab fragment:** The "Fragment Antigen Binding" portion (contains both H and L chains). * **Fc fragment:** The "Fragment Crystallizable" portion (contains only H chains); it determines the biological properties like placental transfer (IgG) or mast cell binding (IgE). * **Hinge Region:** The flexible segment of the heavy chain that allows the Fab arms to move; it is rich in **proline** and **cysteine**. * **Papain Digestion:** Cleaves the antibody into **two Fab** fragments and **one Fc** fragment. * **Pepsin Digestion:** Cleaves it into one **F(ab')2** fragment and degraded Fc fragments.

Q: Which bacteria's antigen cross-reacts with Proteus antigen?

Rickettsiae and Klebsiella. The correct answer is **B. Rickettsiae and Klebsiella**. ### **Explanation** This question refers to the phenomenon of **antigenic cross-reactivity**, where antibodies produced against one organism react with the antigens of a different, unrelated organism due to shared epitopes. 1. **Rickettsiae and Proteus (Weil-Felix Reaction):** This is a classic example of heterophile antibody reaction. Certain strains of *Proteus vulgaris* (OX-19, OX-2) and *Proteus mirabilis* (OX-K) share alkali-stable carbohydrate antigens with various species of *Rickettsia*. In the **Weil-Felix test**, a patient's serum is tested for agglutination against these Proteus antigens to diagnose Rickettsial diseases (e.g., Epidemic typhus, Scrub typhus). 2. **Klebsiella and Proteus:** Cross-reactivity has been documented between *Klebsiella pneumoniae* and *Proteus* species. Specifically, studies in patients with **Ankylosing Spondylitis** have shown cross-reactivity involving *Klebsiella* antigens, *Proteus* antigens, and the HLA-B27 molecule (molecular mimicry). ### **Why other options are incorrect:** * **A & D (Klebsiella/E. coli):** While *E. coli* and *Klebsiella* are both Enterobacteriaceae, they do not share the specific diagnostic cross-reactivity with *Proteus* that is characteristic of *Rickettsia*. * **C (Chlamydiae):** Chlamydiae are obligate intracellular bacteria but do not share common antigens with *Proteus*. Diagnosis is usually via NAAT or Giemsa stain. ### **High-Yield Clinical Pearls for NEET-PG:** * **Weil-Felix Patterns:** * **Scrub Typhus (*O. tsutsugamushi*):** Positive for **OX-K** only. * **Epidemic/Endemic Typhus:** Positive for **OX-19**. * **Rocky Mountain Spotted Fever:** Positive for **OX-19 and OX-2**. * **Q Fever:** Weil-Felix test is **Negative**. * **Molecular Mimicry:** Remember the link between *Klebsiella* and Ankylosing Spondylitis (HLA-B27) as a frequent "match the following" topic.

Q: Which category of hypersensitivity involves complement activation?

Type II and Type III. **Explanation** Hypersensitivity reactions are classified by the Gell and Coombs system based on the underlying immune mechanism. Complement activation is a hallmark of both **Type II** and **Type III** hypersensitivity. * **Type II (Cytotoxic):** Antibodies (IgG or IgM) bind to antigens on the surface of specific cells or tissues. This antigen-antibody complex activates the **classical complement pathway**, leading to the formation of the Membrane Attack Complex (MAC) and cell lysis (e.g., Autoimmune Hemolytic Anemia). * **Type III (Immune-Complex):** Soluble antigens bind to antibodies, forming circulating immune complexes. These complexes deposit in tissues (like blood vessel walls or glomeruli) and trigger **complement activation**. This recruits neutrophils, leading to tissue damage (e.g., SLE, Post-streptococcal Glomerulonephritis). **Why other options are incorrect:** * **Type I:** Mediated by IgE binding to mast cells; involves histamine release, not complement. * **Type IV:** A delayed-type hypersensitivity mediated by T-cells (Th1, Th17, and CD8+), not antibodies or complement. **NEET-PG High-Yield Pearls:** * **Type II** is "Tissue-specific" (Antigen is fixed). * **Type III** is "Systemic" (Antigen is soluble/circulating). * **Complement levels (C3, C4):** Often decreased in Type III reactions (like SLE flares) due to massive consumption during the inflammatory process. * **Mnemonic (ACID):** **A**naphylactic (I), **C**ytotoxic (II), **I**mmune-Complex (III), **D**elayed (IV).

Q: Chediak-Higashi syndrome is characterized by which of the following?

Defect in phagocytosis. **Explanation:** **Chediak-Higashi Syndrome (CHS)** is a rare autosomal recessive disorder caused by a mutation in the **LYST (Lysosomal Trafficking Regulator) gene**. This mutation leads to a defect in microtubule polymerization, which prevents the fusion of phagosomes with lysosomes. 1. **Why Option A is correct:** The hallmark of CHS is the failure of **phagolysosome formation**. While neutrophils can ingest bacteria, they cannot kill them because the digestive enzymes in lysosomes cannot reach the phagosome. This represents a functional **defect in phagocytosis** (specifically the intracellular killing phase). Microscopically, this is visualized as **giant peroxidase-positive granules** in neutrophils, representing fused, dysfunctional lysosomes. 2. **Why other options are incorrect:** * **B. Neutropenia:** While mild neutropenia can occur due to ineffective granulopoiesis, the primary functional pathology defining the disease is the phagocytic defect. * **C & D. Agammaglobulinemia/IgA deficiency:** CHS is a defect of the innate immune system (phagocytes) and natural killer (NK) cells, not a primary B-cell or antibody deficiency. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Tetrad:** Partial oculocutaneous **albinism**, recurrent pyogenic infections (usually *S. aureus*), progressive neurological abnormalities, and mild coagulation defects (bleeding diathesis). * **Diagnosis:** Peripheral blood smear showing **giant lysosomal granules** in neutrophils and melanocytes. * **NK Cell Defect:** Patients also have impaired Natural Killer cell cytotoxicity, increasing susceptibility to viral infections and the "accelerated phase" (hemophagocytic lymphohistiocytosis).

Q: Recurrent Neisseria infections are predisposed by which of the following?

Late complement component deficiency. ### Explanation **Correct Answer: A. Late complement component deficiency** **The Medical Concept:** The complement system is a crucial arm of innate immunity. The **late complement components (C5, C6, C7, C8, and C9)** assemble to form the **Membrane Attack Complex (MAC)**. The MAC is essential for the lysis of Gram-negative bacteria, particularly *Neisseria* species (*N. meningitidis* and *N. gonorrhoeae*), which have thin peptidoglycan layers. Individuals with deficiencies in these components cannot form the MAC, leaving them uniquely susceptible to recurrent, disseminated Neisserial infections. **Analysis of Incorrect Options:** * **B. Properdin deficiency:** Properdin stabilizes the alternative pathway C3 convertase. While its deficiency can increase susceptibility to *Neisseria*, it is much rarer than late component deficiencies and is X-linked. Late component deficiency remains the classic, most high-yield association. * **C. Early complement component deficiency (C1, C4, C2):** These are primarily involved in the classical pathway and the clearance of immune complexes. Deficiencies here typically predispose patients to **Systemic Lupus Erythematosus (SLE)** and pyogenic infections (e.g., *S. pneumoniae*), rather than specific *Neisseria* susceptibility. * **D. C1 esterase deficiency:** This leads to **Hereditary Angioedema** due to the overproduction of bradykinin. It is not associated with an increased risk of bacterial infections. **High-Yield Clinical Pearls for NEET-PG:** * **C3 deficiency:** The most severe complement deficiency; predisposes to recurrent pyogenic infections and Type III hypersensitivity reactions. * **CH50 Assay:** Used to screen for classical pathway and MAC deficiencies. * **Mnemonic:** "Late is for Lysis" — C5-C9 are needed for lysis of *Neisseria*. * **Vaccination:** Patients with terminal complement deficiencies must receive the meningococcal vaccine.

Q: Where are B cells processed?

Bone marrow. **Explanation:** The development of B cells occurs in two distinct phases: **antigen-independent** (maturation) and **antigen-dependent** (activation). **Why Bone Marrow is correct:** In humans, the **Bone Marrow** is the primary lymphoid organ responsible for the generation and maturation of B cells. Here, hematopoietic stem cells undergo gene rearrangement to produce a functional B-cell receptor (BCR). This process is known as "processing" or "central maturation." Once B cells express IgM on their surface (immature B cells), they leave the bone marrow to seed peripheral lymphoid organs. (Note: In birds, this occurs in the *Bursa of Fabricius*, which is the origin of the letter "B" in B cells). **Why other options are incorrect:** * **Liver:** This is the primary site of B-cell production during **fetal life** (extramedullary hematopoiesis). However, in adults, this function shifts entirely to the bone marrow. * **Spleen & Lymph Nodes:** These are **secondary lymphoid organs**. They are sites where mature B cells encounter antigens, undergo activation, and differentiate into plasma cells. They do not "process" or create the B cells initially. **High-Yield Clinical Pearls for NEET-PG:** * **T-cell Processing:** Occurs in the **Thymus**. * **Negative Selection:** The process in the bone marrow where B cells that react strongly to "self-antigens" are eliminated or undergo **receptor editing** to prevent autoimmunity. * **Bruton’s Agammaglobulinemia:** A clinical condition where B-cell maturation is arrested at the pre-B stage due to a mutation in the *Btk* gene, leading to a lack of mature B cells and antibodies.

Q: Which of the following antibodies acts as an opsonin?

IgG. **Explanation:** **1. Why IgG is correct:** Opsonization is the process by which a pathogen is marked for ingestion and destruction by a phagocyte. **IgG** is the only class of antibody that acts as an opsonin. This occurs because the **Fab portion** of the IgG molecule binds to the specific antigen on the pathogen, while the **Fc portion** binds to the **Fcγ receptors (FcγR)** expressed on the surface of phagocytic cells (neutrophils and macrophages). This "bridge" significantly enhances the efficiency of phagocytosis. Specifically, **IgG1 and IgG3** are the most potent opsonins. **2. Why the other options are incorrect:** * **IgM:** While IgM is the most efficient antibody for **complement activation** (via the classical pathway), it does not act as a direct opsonin because phagocytes lack specific receptors for the Fc portion of IgM. * **IgE:** This antibody is primarily involved in **Type I Hypersensitivity** reactions and defense against helminthic parasites by binding to mast cells and basophils. * **IgA:** Found predominantly in secretions (mucosal immunity), IgA prevents the attachment of pathogens to mucosal surfaces (agglutination) but does not function as a classical opsonin for systemic phagocytosis. **Clinical Pearls for NEET-PG:** * **Major Opsonins:** The two most important opsonins in the body are **IgG** and the complement fragment **C3b**. * **IgG Characteristics:** It is the most abundant antibody in serum, the only one to cross the **placenta**, and is responsible for the secondary (anamnestic) immune response. * **Mnemonic:** "Ig**G** **G**rooms the bacteria for eating."

Question 1

The Oudin procedure is a method of immunodiffusion that utilizes which of the following techniques?

Accepted Answer

Single diffusion in one dimension

Answer

Double diffusion in one dimension

Answer

Single diffusion in two dimensions

Answer

Double diffusion in two dimensions

Question 2

The peptide binding site on Class I MHC molecules is located in which region?

Accepted Answer

The distal domain of the alpha subunit

Answer

The proximal domain of the alpha subunit

Answer

The proximal domains of the alpha and beta subunits

Answer

The distal domains of the alpha and beta subunits

Question 3

What is the basic structure of an antibody?

Accepted Answer

Two long and two short peptide chains

Answer

A single peptide chain

Answer

Two peptide chains

Answer

Non-sulfur amino acids

Question 4

Which bacteria's antigen cross-reacts with Proteus antigen?

Accepted Answer

Rickettsiae and Klebsiella

Answer

Klebsiella

Answer

Chlymydiae

Answer

E. coli

Question 5

Which category of hypersensitivity involves complement activation?

Accepted Answer

Type II and Type III

Answer

Type II

Answer

Type III

Answer

Type IV and Type II

Question 6

Chediak-Higashi syndrome is characterized by which of the following?

Accepted Answer

Defect in phagocytosis

Answer

Neutropenia

Answer

Agammaglobulinemia

Answer

IgA deficiency

Question 7

Recurrent Neisseria infections are predisposed by which of the following?

Accepted Answer

Late complement component deficiency

Answer

Properdin deficiency

Answer

Early complement component deficiency

Answer

C1 esterase deficiency

Question 8

Where are B cells processed?

Accepted Answer

Bone marrow

Answer

Liver

Answer

Spleen

Answer

Lymph nodes

Question 9

What is the other name for sex-linked graft rejection?

Accepted Answer

Eichwald Silmser effect

Answer

Schultz-Dale phenomenon

Answer

Shwartzman reaction

Answer

Theobald Smith phenomenon

Question 10

Which of the following antibodies acts as an opsonin?

Accepted Answer

IgG

Answer

IgM

Answer

IgE

Answer

IgA

Immunology — MCQs

Immunology — MCQs

On this page

Practice by Chapter

Want unlimited practice?