Immunology Practice Questions

Q: Which immunoglobulin crosses the placenta maximally?

IgG1. **Explanation:** The transfer of maternal antibodies across the placenta is a selective process mediated by the **neonatal Fc receptor (FcRn)** located on syncytiotrophoblast cells. While IgG is the only class of immunoglobulin that crosses the placenta, the four subclasses (IgG1, IgG2, IgG3, and IgG4) are transported with varying efficiencies. **Why IgG1 is the correct answer:** IgG1 is the most abundant subclass and has the highest affinity for the FcRn receptor. Consequently, it is transported most efficiently and **maximally** across the placenta. By birth, fetal levels of IgG1 often exceed maternal levels, providing the newborn with critical passive immunity against protein antigens (e.g., toxins and viruses). **Analysis of Incorrect Options:** * **IgG2:** This subclass has the **lowest** efficiency of placental transfer. It primarily targets polysaccharide antigens (e.g., *S. pneumoniae*), which explains why neonates are particularly susceptible to encapsulated bacteria. * **IgG3:** While IgG3 crosses the placenta effectively (often ranked second after IgG1), its transport begins slightly later in gestation and it has a shorter half-life compared to IgG1. * **IgG4:** This subclass crosses the placenta with intermediate efficiency, generally higher than IgG2 but significantly lower than IgG1. **NEET-PG High-Yield Pearls:** * **Order of Placental Transfer:** IgG1 > IgG3 > IgG4 > IgG2. * **Timing:** Transfer begins as early as the 13th week but occurs primarily during the **third trimester**. * **Exception:** IgG is the *only* immunoglobulin to cross the placenta; IgM, IgA, IgD, and IgE do not. * **Clinical Correlation:** Congenital infections (TORCH) are often diagnosed by detecting **IgM** in the neonate, as maternal IgM cannot cross the placenta.

Q: Which of the following immunoglobulins has the highest mean serum concentration in humans?

IgG. **Explanation:** The correct answer is **IgG**. In healthy adults, IgG is the most abundant class of immunoglobulin, accounting for approximately **75–80%** of the total serum antibodies. Its high concentration (800–1600 mg/dL) is due to its long half-life (about 21 days) and its role as the primary mediator of the secondary immune response. **Why the other options are incorrect:** * **IgA (Option A):** It is the second most common serum immunoglobulin (~15%). While it is the most abundant antibody in **secretions** (tears, saliva, colostrum), its serum levels are significantly lower than IgG. * **IgM (Option B):** It accounts for about 5–10% of serum antibodies. It is the largest in size (pentamer) and the first to appear in a primary immune response, but it has a shorter half-life and lower concentration than IgG. * **IgD (Option D):** It is found in trace amounts in the serum ( IgA > IgM > IgD > IgE**. * **Placental Transfer:** IgG is the **only** immunoglobulin that crosses the placenta, providing passive immunity to the fetus. * **Complement Activation:** IgM is the most potent activator of the classical complement pathway (due to its pentameric structure), followed by IgG. * **Multiple Myeloma:** IgG is the most common monoclonal protein (M-spike) found in Multiple Myeloma, followed by IgA.

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

Bacterial surface polysaccharide. ### Explanation The complement system is a crucial component of innate immunity, consisting of a cascade of proteins that lead to pathogen opsonization and lysis. It can be activated via three distinct pathways: **1. Why Option C is Correct:** The **Alternative Pathway** is unique because it does not require antibodies for activation. It is triggered directly by the surfaces of various infectious agents. **Bacterial surface polysaccharides** (such as Lipopolysaccharide/LPS from Gram-negative bacteria), teichoic acid, fungal cell walls (zymosan), and certain viruses act as triggers. This pathway involves the spontaneous hydrolysis of C3 and the participation of **Factors B, D, and Properdin**. **2. Why Other Options are Incorrect:** * **Option A (Antigen-Antibody complex):** This is the primary trigger for the **Classical Pathway**. It specifically requires IgG (IgG1, IgG2, IgG3) or IgM bound to an antigen to initiate the C1 complex. * **Option B (Mannose-binding lectin):** This triggers the **Lectin Pathway**. It occurs when MBL (a pattern recognition receptor) binds to mannose residues on the surface of pathogens like *Salmonella* or *Candida*. **High-Yield Clinical Pearls for NEET-PG:** * **C3** is the most abundant complement protein and the common point where all three pathways converge. * **C3b** is the major **opsonin** (enhances phagocytosis). * **C5a** is the most potent **chemotactic** agent and anaphylatoxin. * **C5b-9** forms the **Membrane Attack Complex (MAC)**, which causes osmotic lysis of the cell. * **Deficiency of Properdin/Alternative pathway** increases susceptibility to *Neisseria* infections.

Q: What is the primary function of MHC Class I, Class II, and Class III molecules?

Cytokines and complement system components.. The Major Histocompatibility Complex (MHC) is a set of genes located on the short arm of Chromosome 6. Understanding their distinct roles is high-yield for NEET-PG. **Explanation of the Correct Answer:** The question asks for the primary functions of the three classes. While MHC I and II are involved in antigen presentation, **MHC Class III** is unique because it does not present antigens. Instead, it encodes for various secreted proteins, primarily **complement system components** (C2, C4, Factor B) and **cytokines** like Tumor Necrosis Factor (TNF-α and TNF-β). Therefore, Option C correctly identifies the functional output of the MHC III region. **Analysis of Incorrect Options:** * **Option A & B:** These confuse the pathways of MHC I and II. **MHC Class I** presents **intracellular** (endogenous) antigens to CD8+ T-cells. **MHC Class II** presents **extracellular** (exogenous) antigens to CD4+ T-cells. While these cover Classes I and II, they do not accurately describe Class III. * **Option D:** This is an incomplete description. While macrophages express MHC II, antigen presentation occurs *to* T-lymphocytes, not *to* macrophages. **High-Yield NEET-PG Pearls:** * **MHC I:** Found on all nucleated cells (not RBCs). Associated with HLA-A, B, and C. * **MHC II:** Found only on Professional Antigen Presenting Cells (APCs) like Dendritic cells, B-cells, and Macrophages. Associated with HLA-DP, DQ, and DR. * **MHC III:** Does not participate in graft rejection (unlike I and II). * **Rule of 8:** MHC I × CD8 = 8; MHC II × CD4 = 8. This helps remember which T-cell binds to which MHC.

Q: Which of the following is a HLA class III molecule?

TNF-α. **Explanation:** The Human Leukocyte Antigen (HLA) complex is located on the short arm of **Chromosome 6**. It is divided into three classes based on structure and function. **1. Why TNF-α is the Correct Answer:** While HLA Class I and II molecules are primarily involved in antigen presentation, **HLA Class III** molecules are a diverse group of proteins that do not present antigens. Instead, they are involved in the inflammatory response and the complement system. Key Class III molecules include: * **Cytokines:** Tumor Necrosis Factor-alpha (**TNF-α**) and Lymphotoxin (TNF-β). * **Complement components:** C2, C4A, C4B, and Factor B. * **Heat Shock Proteins:** HSP70. **2. Why the Other Options are Incorrect:** * **HLA-G (Option A):** This is a **Non-classical HLA Class I** molecule (Class Ib). It is primarily expressed on cytotrophoblasts at the feto-maternal interface and plays a crucial role in immune tolerance during pregnancy. * **HLA-H (Option B):** This is a **pseudogene** related to Class I. Note: The *HFE* gene (associated with Hemochromatosis) was formerly called HLA-H, but it remains a Class I-like structure. **High-Yield Clinical Pearls for NEET-PG:** * **Class I (A, B, C):** Present endogenous antigens to **CD8+ T cells**. * **Class II (DR, DQ, DP):** Present exogenous antigens to **CD4+ T cells**. * **Class III:** Unique because they are **not** membrane-bound surface markers; they are secreted proteins. * **MHC Restriction:** CD4 cells recognize MHC II; CD8 cells recognize MHC I (Rule of 8: 4×2=8 and 8×1=8).

Q: Which immunoglobulin is inactivated by heating and elevated in helminthic infections?

IgE. **Explanation:** The correct answer is **IgE**. This immunoglobulin is uniquely characterized by its **heat-lability** and its role in Type I hypersensitivity and parasitic defense. **Why IgE is correct:** * **Heat Sensitivity:** IgE is the most heat-labile immunoglobulin. Heating serum to **56°C for 30 to 60 minutes** inactivates IgE by denaturing the Fc portion of the heavy chain, preventing it from binding to mast cells (the Prausnitz-Küstner reaction becomes negative). * **Helminthic Infections:** IgE levels rise significantly during helminthic infestations. It mediates **Antibody-Dependent Cellular Cytotoxicity (ADCC)** by coating the parasite; eosinophils then bind to the IgE via FcεRI receptors and release major basic protein to kill the helminth. **Why other options are incorrect:** * **IgA:** The primary secretory antibody found in colostrum and mucosal surfaces. It is heat-stable and primarily involved in preventing pathogen attachment to mucosal linings. * **IgG:** The most abundant serum antibody and the only one to cross the placenta. It is heat-stable and involved in secondary immune responses and opsonization. * **IgM:** The largest (pentameric) antibody and the first to appear in primary infection. While it is efficient at complement fixation, it is not inactivated by standard heating at 56°C. **High-Yield NEET-PG Pearls:** * **Reaginic Antibody:** IgE is also known as the reaginic antibody. * **Homocytotropism:** IgE has a high affinity for mast cells and basophils. * **Lowest Serum Concentration:** It is the immunoglobulin present in the lowest concentration in normal serum. * **Structure:** It is a monomer with an extra constant domain (CH4) on its heavy chain.

Q: What is the functional surface molecule on T-lymphocytes that facilitates antigen recognition by Major Histocompatibility Complex (MHC) molecules?

T8. **Explanation:** The question focuses on the interaction between T-lymphocytes and the Major Histocompatibility Complex (MHC). T-lymphocytes recognize antigens only when presented by MHC molecules. This process is facilitated by specific co-receptors: **CD4** (T4) and **CD8** (T8). **Why T8 is the correct answer:** The **T8 (CD8)** molecule is a transmembrane glycoprotein found on cytotoxic T-cells. It acts as a co-receptor that specifically binds to the non-polymorphic region of **MHC Class I** molecules. This binding stabilizes the interaction between the T-cell receptor (TCR) and the antigen-MHC complex, facilitating signal transduction and subsequent immune response. **Analysis of Incorrect Options:** * **A. T4 (CD4):** While T4 also facilitates MHC recognition, it specifically binds to **MHC Class II** molecules on helper T-cells. In many exam contexts, if the question implies MHC Class I or general cytotoxic function, T8 is the specific focus. * **B. T11 (CD2):** This is an adhesion molecule found on T-cells and NK cells. Its primary role is binding to LFA-3 on antigen-presenting cells to stabilize cell-to-cell contact, but it does not directly facilitate MHC-specific antigen recognition. * **C. T3 (CD3):** This is a complex of proteins associated with the T-cell receptor (TCR). While essential for **signal transduction** once an antigen is recognized, it does not "facilitate recognition" by binding to the MHC molecule itself. **High-Yield Clinical Pearls for NEET-PG:** * **MHC Restriction Rule:** Remember the **"Rule of 8"**: CD4 × MHC 2 = 8; CD8 × MHC 1 = 8. * **CD3** is the definitive marker for all T-lymphocytes. * **CD2 (T11)** is used in the "E-rosette" test to identify T-cells (historical diagnostic significance).

Q: Recurrent facial, oropharyngeal, or laryngeal edema in a patient is associated with low C4, normal C3, and normal Factor B. The pathogenesis is most likely due to:

C1 esterase inhibitor deficiency. ### Explanation The clinical presentation of recurrent facial, oropharyngeal, or laryngeal edema without urticaria is characteristic of **Hereditary Angioedema (HAE)**, which is caused by a deficiency or dysfunction of the **C1 esterase inhibitor (C1-INH)**. **Why the correct answer is right:** C1-INH normally inhibits the C1 complex and the kallikrein-kinin system. In its absence, there is uncontrolled activation of C1, leading to the continuous consumption of **C4** and **C2**. This results in **persistently low C4 levels**, even between attacks. Because C1-INH also regulates the conversion of kininogen to **bradykinin**, its deficiency leads to excessive bradykinin, causing increased vascular permeability and edema. **C3 levels remain normal** because the activation does not proceed to the C3 convertase level in a significant way, and **Factor B** is normal because the alternative pathway is not involved. **Why incorrect options are wrong:** * **Option A & D:** Immune complex diseases (e.g., SLE) or IgM-mediated activation involve the consumption of the entire classical pathway. This would typically result in **low C3** in addition to low C4. * **Option C:** While C2 deficiency is a complement disorder, it does not cause angioedema. It usually presents with SLE-like features or recurrent pyogenic infections. **NEET-PG High-Yield Pearls:** * **Screening Test of Choice:** Serum **C4 level** (it is almost always low in HAE). * **Confirmatory Test:** C1-INH antigenic levels or functional assay. * **Key Mediator:** Bradykinin (NOT histamine; hence, HAE does not respond to antihistamines or steroids). * **Management:** Acute attacks are treated with **C1-INH concentrate** or **Icatibant** (bradykinin B2 receptor antagonist). Prophylaxis includes **Danazol** (stanozolol) or Tranexamic acid.

Q: CRP is an acute-phase protein in inflammatory processes. What is the expansion of 'C' in CRP?

Capsular polysaccharide of pneumococcus. **Explanation:** **C-Reactive Protein (CRP)** is a classic acute-phase reactant synthesized by the liver in response to inflammatory cytokines, primarily **Interleukin-6 (IL-6)**. **Why Option C is Correct:** The protein was first discovered by Tillett and Francis in 1930. They observed that the serum of patients with pneumonia contained a substance that reacted and formed a precipitate with the **'C' polysaccharide** (a phosphocholine-containing carbohydrate) found in the **capsule/cell wall of *Streptococcus pneumoniae***. Thus, the 'C' in CRP stands for the **Capsular polysaccharide of pneumococcus**. **Analysis of Incorrect Options:** * **Option A (Concanavalin A):** This is a lectin (plant protein) derived from the jack bean, used in labs as a lymphocyte mitogen; it has no relation to the naming of CRP. * **Option B (Chondroitin sulfate):** This is a glycosaminoglycan found in cartilage; the "series with ARP, BRP" is a distractor with no medical basis. * **Option D (Cellular):** CRP is a plasma protein (humoral component), not a cellular component. **High-Yield Clinical Pearls for NEET-PG:** * **Function:** CRP acts as an **opsonin**, activating the classical complement pathway by binding to C1q. * **Kinetics:** It rises rapidly (within 6–12 hours) and has a short half-life (19 hours), making it a sensitive indicator of **current** inflammation or infection. * **hs-CRP (high-sensitivity CRP):** Used as a biomarker for chronic low-grade inflammation and is a significant predictor of **Cardiovascular Risk**. * **Diagnostic Value:** It is a non-specific marker; it indicates that inflammation is present but does not identify the specific cause.

Question 1

What is true about Hybridoma?

Accepted Answer

It immortalises myeloma cells.

Answer

Hybridoma cells are produced by the fusion of B-cells and myeloma cells.

Answer

The cell is of human origin.

Answer

Prior immunisation is done.

Question 2

Which immunoglobulin crosses the placenta maximally?

Accepted Answer

IgG1

Answer

IgG2

Answer

IgG3

Answer

IgG4

Question 3

Which of the following immunoglobulins has the highest mean serum concentration in humans?

Accepted Answer

IgG

Answer

IgA

Answer

IgD

Answer

IgM

Question 4

Which of the following activates the alternative complement pathway?

Accepted Answer

Bacterial surface polysaccharide

Answer

Antigen-Antibody complex

Answer

Mannose-binding lectin

Answer

All of the above

Question 5

What is the primary function of MHC Class I, Class II, and Class III molecules?

Accepted Answer

Cytokines and complement system components.

Answer

Intracellular antigens, extracellular antigens, and complement system.

Answer

Extracellular antigens, intracellular antigens, and toxins.

Answer

Antigen presentation to macrophages.

Question 6

Which of the following is a HLA class III molecule?

Accepted Answer

TNF-α

Answer

HLA-G

Answer

HLA-H

Answer

None of the above

Question 7

Which immunoglobulin is inactivated by heating and elevated in helminthic infections?

Accepted Answer

IgE

Answer

IgA

Answer

IgG

Answer

IgM

Question 8

What is the functional surface molecule on T-lymphocytes that facilitates antigen recognition by Major Histocompatibility Complex (MHC) molecules?

Accepted Answer

T8

Answer

T4

Answer

T11

Answer

T3

Question 9

Recurrent facial, oropharyngeal, or laryngeal edema in a patient is associated with low C4, normal C3, and normal Factor B. The pathogenesis is most likely due to:

Accepted Answer

C1 esterase inhibitor deficiency

Answer

Immune complex disease

Answer

Hereditary deficiency of C2

Answer

Classical pathway activation by IgM

Question 10

CRP is an acute-phase protein in inflammatory processes. What is the expansion of 'C' in CRP?

Accepted Answer

Capsular polysaccharide of pneumococcus

Answer

Concanavalin A

Answer

Chondroitin sulfate in series with ARP, BRP

Answer

Cellular

Immunology — MCQs

Immunology — MCQs

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