Immunology Practice Questions

Q: What is the process that increases the ability for phagocytosis of foreign bodies by the body?

Opsonization. ### Explanation **Correct Answer: B. Opsonization** **Opsonization** is the process by which foreign particles (like bacteria) are coated with specific proteins called **opsonins**, making them more "palatable" and easily recognized by phagocytes (macrophages and neutrophils). * **Mechanism:** Phagocytes have receptors for the Fc portion of IgG and the C3b component of the complement system. When these opsonins bind to an antigen, they act as a bridge, allowing the phagocyte to bind firmly to the target, significantly enhancing the efficiency of ingestion. **Why other options are incorrect:** * **A. Cross-reactivity:** This occurs when an antibody raised against one specific antigen binds to a different but structurally similar antigen (e.g., *Streptococcus pyogenes* antibodies reacting with human heart tissue in Rheumatic Fever). It does not directly enhance phagocytosis. * **C. Immune Tolerance:** This is the state of unresponsiveness of the immune system to specific antigens, particularly "self-antigens," to prevent autoimmunity. * **D. Immune Surveillance:** This is the continuous monitoring process by which the immune system (primarily NK cells and T-cells) identifies and destroys nascent tumor cells or virally infected cells. **High-Yield Clinical Pearls for NEET-PG:** * **Most potent opsonins:** **IgG** (specifically IgG1 and IgG3) and **C3b**. * **Acute Phase Reactant:** C-Reactive Protein (CRP) also acts as an opsonin. * **Clinical Correlation:** Patients with **splenectomy** or **complement deficiencies** (C3) have impaired opsonization, leading to increased susceptibility to encapsulated organisms like *S. pneumoniae*, *H. influenzae*, and *N. meningitidis*. * **Mnemonic:** **O**psonization **P**repares the food for **P**hagocytosis.

Q: Which of the following statements about NK cells is INCORRECT?

Mediates type IV hypersensitivity. ### Explanation **Correct Answer: A. Mediates type IV hypersensitivity** **Why Option A is Incorrect (The Right Choice):** Type IV (Delayed-type) hypersensitivity is primarily mediated by **T-lymphocytes** (specifically CD4+ Th1 cells and CD8+ T cells), not NK cells. In Type IV reactions, sensitized T-cells release cytokines that activate macrophages or cause direct cytotoxicity. NK cells are part of the **innate immune system**, whereas Type IV hypersensitivity is a component of the **adaptive immune response**. **Analysis of Other Options:** * **Option B (Kills virus-infected cells):** This is a primary function of NK cells. They identify and destroy cells that have downregulated MHC-I molecules (the "missing self" hypothesis), a common tactic used by viruses to evade CD8+ T-cells. * **Option C (Large granular lymphocytes):** Morphologically, NK cells are identified as large granular lymphocytes (LGLs). They are larger than resting B or T cells and contain prominent cytoplasmic granules. * **Option D (Releases perforin and granzyme):** NK cells utilize the perforin-granzyme pathway to induce apoptosis in target cells. Perforin creates pores in the target cell membrane, allowing granzymes (proteases) to enter and trigger the caspase cascade. **High-Yield Clinical Pearls for NEET-PG:** * **Markers:** NK cells are typically identified by the presence of **CD56** and **CD16** (FcγRIII) and the **absence of CD3**. * **Antibody-Dependent Cellular Cytotoxicity (ADCC):** NK cells use their CD16 receptor to bind to the Fc portion of IgG-coated target cells, leading to cell lysis. * **Cytokine Production:** They are a major source of **IFN-gamma**, which activates macrophages. * **MHC Restriction:** Unlike T-cells, NK cells are **not MHC-restricted**; they do not require antigen presentation via MHC to function.

Q: Which of the following statements about complement is false?

Constitutes about 20% of normal serum proteins. ### Explanation **1. Why Option B is the Correct (False) Statement:** The complement system consists of a group of approximately 30 proteins, but they constitute only about **10% of the total serum globulin fraction** (or roughly **5% of total serum proteins**). Stating that they make up 20% is a significant overestimation, making this the false statement. **2. Analysis of Other Options:** * **Option A (Group of proteins normally found in serum):** This is true. Complement proteins are synthesized primarily by the liver (and also by macrophages) and circulate in an inactive (pro-enzyme) form in the blood. * **Option C (Heat labile):** This is true. Complement is highly sensitive to heat. It is inactivated when serum is heated at **56°C for 30 minutes**. This property is used in laboratories to "inactivate" serum before certain serological tests. * **Option D (Species non-specific):** This is true. Unlike antibodies, which are specific to the antigen and the species that produced them, complement from one species (e.g., guinea pig) can react with antibodies from another species (e.g., human) to cause lysis. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Most Abundant Component:** **C3** is the most abundant complement protein in the serum. * **Pathways:** There are three pathways—Classical (triggered by Ag-Ab complexes), Alternative (triggered by endotoxins/microbial surfaces), and Lectin (triggered by mannose-binding lectin). * **C3b:** Acts as a powerful **opsonin** (enhances phagocytosis). * **C5a:** The most potent **anaphylatoxin** and chemotactic agent. * **Membrane Attack Complex (MAC):** Formed by **C5b-C9**, responsible for cell lysis. * **Deficiency:** C3 deficiency is the most severe as it is the "bottleneck" of all pathways, leading to recurrent pyogenic infections.

Q: On which component of the complement system does C3 convertase act?

C3. **Explanation:** The complement system is a biochemical cascade of the innate immune system. The central event in all three pathways (Classical, Alternative, and Lectin) is the formation of **C3 convertase**. **Why Option A is correct:** C3 convertase is an enzyme complex whose specific substrate is the **C3 protein**. It cleaves C3 into two fragments: **C3a** (an anaphylatoxin) and **C3b** (an opsonin). This step is the "amplification loop" of the complement cascade, as one molecule of C3 convertase can cleave hundreds of C3 molecules, leading to massive deposition of C3b on the pathogen surface. **Why other options are incorrect:** * **Option B (C4b2b):** This is not a substrate; it is the **Classical/Lectin pathway C3 convertase** itself. It acts *on* C3, it is not acted upon by C3 convertase. * **Option C (C4b):** This is a fragment of C4 that combines with C2b to form the C3 convertase complex. It is a structural component, not the primary substrate of the convertase. * **Option D (Lymphocytosis):** This refers to an increased lymphocyte count in the blood, typically seen in viral infections or chronic lymphocytic leukemia. It is unrelated to the biochemical mechanism of the complement system. **High-Yield Clinical Pearls for NEET-PG:** * **C3 Convertase Compositions:** * Classical/Lectin Pathway: **C4b2b** (formerly C4b2a). * Alternative Pathway: **C3bBb**. * **C5 Convertase:** Formed when C3b binds to C3 convertase (C4b2b3b or C3bBb3b). * **MAC (Membrane Attack Complex):** Initiated by C5b and consists of **C5b-C9**. * **Deficiency:** C3 deficiency is the most severe complement deficiency, leading to recurrent pyogenic infections and Type III hypersensitivity reactions.

Q: CD4 cells recognize antigens in association with which of the following?

MHC II. **Explanation:** The recognition of antigens by T-lymphocytes is governed by the principle of **MHC Restriction**. T-cells do not recognize free-floating antigens; instead, they only recognize peptide fragments presented on **Major Histocompatibility Complex (MHC)** molecules. * **Why MHC II is correct:** CD4+ T-cells (Helper T-cells) specifically recognize exogenous antigens presented by **MHC Class II** molecules. These molecules are found exclusively on **Professional Antigen-Presenting Cells (APCs)** such as macrophages, B-cells, and dendritic cells. A helpful mnemonic is the **"Rule of 8"**: * CD**4** × MHC **II** = 8 * CD**8** × MHC **I** = 8 **Analysis of Incorrect Options:** * **A. MHC I:** These molecules are expressed on all nucleated cells and present endogenous antigens (e.g., viral or tumor proteins) to **CD8+ Cytotoxic T-cells**. * **C. MHC III:** These genes encode various components of the innate immune system, such as complement proteins (C2, C4) and cytokines (TNF-α), but they are not involved in antigen presentation to T-cells. * **D. B-cell receptor (BCR):** This is a membrane-bound antibody (IgM/IgD) on B-cells that recognizes free, native antigens directly without the need for MHC presentation. **High-Yield Clinical Pearls for NEET-PG:** * **MHC Class II Structure:** Composed of two polypeptide chains (α and β) of roughly equal size. * **Invariant Chain:** This protein prevents premature binding of self-proteins to MHC II while it is in the Endoplasmic Reticulum. * **HLA Association:** MHC II is encoded by the **HLA-DP, DQ, and DR** loci on Chromosome 6. * **Exogenous Pathway:** MHC II is associated with the endocytic pathway, where extracellular pathogens are internalized and degraded in lysosomes.

Q: What is true about MHC Class I?

Class III has complement. The Major Histocompatibility Complex (MHC), known as Human Leukocyte Antigen (HLA) in humans, is a cluster of genes located on the **short arm of Chromosome 6**. It is divided into three classes based on structure and function. **Explanation of the Correct Option:** * **Option B (Correct):** The MHC Class III region is located between Class I and Class II loci. Unlike Class I and II, it does not encode antigen-presenting molecules. Instead, it encodes various secreted proteins with immune functions, most notably **complement components (C2, C4A, C4B)** and **Factor B**, as well as cytokines like TNF-α and TNF-β. **Analysis of Incorrect Options:** * **Option A:** MHC genes are located on **Chromosome 6**, not Chromosome 4. * **Option C:** The **Class I** region comprises the **A, B, and C loci**. Class II comprises the **DP, DQ, and DR** loci. * **Option D:** The **Mixed Leukocyte Reaction (MLR)** is primarily a measure of **MHC Class II** incompatibility (specifically the HLA-DR locus), which triggers T-helper cell proliferation. Class I is primarily involved in the effector phase of graft rejection. **High-Yield Clinical Pearls for NEET-PG:** * **MHC Class I:** Found on all nucleated cells; presents endogenous antigens to **CD8+ T-cells**. * **MHC Class II:** Found only on Professional Antigen Presenting Cells (APCs) like B-cells, macrophages, and dendritic cells; presents exogenous antigens to **CD4+ T-cells**. * **Structure:** Class I consists of one heavy chain and a **β2-microglobulin** (encoded on Chromosome 15). Class II consists of two heavy chains (α and β). * **Ankylosing Spondylitis:** Strongly associated with **HLA-B27** (a Class I allele).

Q: Regarding IgE, which of the following statements is false?

Crosses the placenta. ### Explanation The correct answer is **D. Crosses the placenta**. This statement is false because **IgG** is the only immunoglobulin class capable of crossing the placental barrier to provide passive immunity to the fetus. #### Why the correct answer is right: IgE is a monomeric antibody with a high molecular weight and a specific Fc region that binds to mast cells and basophils rather than placental receptors (neonatal Fc receptors or FcRn). Only IgG subclasses (IgG1, IgG3, and IgG4) possess the necessary transport mechanisms to cross the placenta. #### Why the other options are wrong: * **A & B (Causes anaphylaxis / Mediates immediate hypersensitivity):** These are true statements. IgE is the primary mediator of **Type I Hypersensitivity** reactions. Upon re-exposure to an allergen, the allergen cross-links IgE molecules already bound to the surface of mast cells and basophils, leading to degranulation and the release of inflammatory mediators like histamine. * **C (Fixes complement):** This is generally considered a false property of IgE, but in the context of this multiple-choice question, "Crosses the placenta" is the *most* definitive false statement. IgE does **not** activate the classical complement pathway (only IgM and IgG do). #### High-Yield Clinical Pearls for NEET-PG: * **Heat Lability:** IgE is the most heat-labile immunoglobulin (inactivated at 56°C for 1 hour). * **Prausnitz-Küstner (PK) Reaction:** Historically used to detect IgE-mediated hypersensitivity. * **Serum Levels:** IgE has the lowest serum concentration and the shortest half-life (~2 days) among all immunoglobulins. * **Role in Parasites:** IgE plays a crucial role in immunity against helminthic infections via **Eosinophil-mediated ADCC** (Antibody-Dependent Cellular Cytotoxicity). * **Receptor:** It binds to high-affinity **FcεRI** receptors on mast cells.

Question 1

What is the process that increases the ability for phagocytosis of foreign bodies by the body?

Accepted Answer

Opsonization

Answer

Cross reactivity

Answer

Immune Tolerance

Answer

Immune Surveillance

Question 2

Which of the following statements about NK cells is INCORRECT?

Accepted Answer

Mediates type IV hypersensitivity

Answer

Kills virus-infected cells

Answer

They are large granular lymphocytes

Answer

Releases small cytoplasmic granules of proteins called perforin and granzyme

Question 3

Which of the following statements about complement is false?

Accepted Answer

Constitutes about 20% of normal serum proteins

Answer

Group of proteins normally found in serum

Answer

Heat labile

Answer

Species non-specific

Question 4

On which component of the complement system does C3 convertase act?

Accepted Answer

C3

Answer

C4b2b

Answer

C4b

Answer

Lymphocytosis

Question 5

CD4 cells recognize antigens in association with which of the following?

Accepted Answer

MHC II

Answer

MHC I

Answer

MHC III

Answer

B-cell receptor

Question 6

Which of the following statements regarding superantigens is NOT true?

Accepted Answer

They bind to the cleft (antigen binding groove) in the MHC class II molecule.

Answer

They bind directly to both MHC class II molecules and T cell receptors, causing T cell activation.

Answer

They bind directly to the lateral aspect of the T cell receptor.

Answer

They bind to T cells irrespective of the antigen specificity of the T cell receptor.

Question 7

What is the major role of HLA class III region genes?

Accepted Answer

Governing susceptibility to autoimmune diseases

Answer

Immune surveillance

Answer

Transplant rejection phenomenon

Answer

Antigen presentation and elimination

Question 8

What is true about MHC Class I?

Accepted Answer

Class III has complement

Answer

Present on chromosome 4

Answer

Class II comprises A, B, C loci

Answer

Class I is involved in mixed leucocyte reaction

Question 9

In a patient with a Salmonella infection, which of the following mechanisms will most likely be the earliest adaptive response for clearing the infection while bacteria are present within intracellular endosomes?

Accepted Answer

Delayed-type hypersensitivity (DTH) responses generated by CD4+ T cells

Answer

Antibody mediated neutralization of free bacteria

Answer

Complement mediated lysis of infected host cells

Answer

Cytotoxic T-lymphocyte (CTL) recognition of bacterial peptides presented by MHC class II

Question 10

Regarding IgE, which of the following statements is false?

Accepted Answer

Crosses the placenta

Answer

Causes anaphylaxis

Answer

Mediates immediate hypersensitivity reactions

Answer

Fixes complement

Immunology — MCQs

Immunology — MCQs

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