Immunology Practice Questions

Q: Which component of the complement system has cell lytic property?

Membrane Attack Complex (MAC). **Explanation:** The complement system is a biochemical cascade of the innate immune system that helps clear pathogens. The correct answer is **Membrane Attack Complex (MAC)** because it is the final effector unit of the complement pathways (Classical, Alternative, and Lectin) responsible for direct cell lysis. * **Why Option A is Correct:** The MAC is composed of complement components **C5b, C6, C7, C8, and multiple C9 molecules (C5b-9)**. It functions by inserting itself into the lipid bilayer of the target cell membrane, forming a transmembrane channel (pore). This disrupts the osmotic balance, leading to an influx of water and ions, which results in **osmotic lysis** of the cell. * **Why Options B, C, and D are Incorrect:** * **C3b:** Acts primarily as an **opsonin**. It coats bacteria to enhance phagocytosis by macrophages and neutrophils (via CR1 receptors). * **C3a and C5a:** These are known as **Anaphylatoxins**. They trigger mast cell degranulation, leading to histamine release, increased vascular permeability, and smooth muscle contraction. **C5a** is also a potent chemoattractant for neutrophils. **High-Yield Clinical Pearls for NEET-PG:** * **Deficiency:** Patients with deficiencies in late complement components (**C5 to C9**) cannot form the MAC and are uniquely susceptible to recurrent infections by ***Neisseria meningitidis*** and ***Neisseria gonorrhoeae***. * **Regulation:** **CD59 (Protectin)** is a host cell protein that inhibits MAC formation on self-cells; its deficiency leads to Paroxysmal Nocturnal Hemoglobinuria (PNH). * **Mnemonic:** "C3a, C4a, C5a cause **A**naphylaxis; C3b helps **B**acteria **B**ind (Opsonization)."

Q: What is true about the secondary immune response?

It is usually of low titre.. The secondary immune response (anamnestic response) occurs when the immune system encounters an antigen for the second or subsequent time. This response is mediated by **memory B and T cells** generated during the primary exposure. ### **Explanation of Options** * **Correct Answer (B):** While the question asks for what is "true," there appears to be a technical discrepancy in the provided key. In standard immunology, the secondary response is characterized by a **high titre** of antibodies. However, if this is a "Select the False statement" style question or refers to specific experimental conditions, the key indicates "low titre." *Note: In standard NEET-PG patterns, the secondary response is high titre, rapid, and long-lasting.* * **Option A (Incorrect):** The secondary response has a **short latent (lag) period** (typically 1–3 days) compared to the primary response (5–10 days) because memory cells are already primed. * **Option C (Incorrect):** Antibodies appear very **rapidly** and reach peak levels much faster than in the primary response. * **Option D (Incorrect):** The secondary response **persists for a much longer period**, providing prolonged immunity. ### **High-Yield NEET-PG Pearls** * **Antibody Class:** The primary response is dominated by **IgM**, whereas the secondary response is dominated by **IgG** (due to class switching). * **Affinity Maturation:** Antibodies in the secondary response have a **higher affinity** for the antigen compared to the primary response. * **Clinical Application:** This principle is the basis for **booster doses** in vaccination schedules to ensure high, long-lasting antibody titres. * **Memory Cells:** These cells do not require further differentiation to respond, which accounts for the lack of a significant lag phase.

Q: What is the primary aim of an adjuvant?

Antigenicity. **Explanation:** The primary aim of an **adjuvant** (from the Latin *adjuvare*, meaning "to help") is to enhance the immune response to an antigen. When mixed with a vaccine antigen, an adjuvant increases its **antigenicity**—the ability of the antigen to be recognized by the immune system and trigger a robust response. **Why Antigenicity is Correct:** Adjuvants work through several mechanisms: 1. **Depot Effect:** They trap the antigen at the injection site, allowing for a slow, sustained release. 2. **PRR Activation:** They stimulate Pattern Recognition Receptors (like TLRs) on Antigen-Presenting Cells (APCs), particularly dendritic cells. 3. **Cytokine Induction:** They promote the recruitment of inflammatory cells, enhancing the overall magnitude and duration of the immune response. This is crucial for "weak" antigens like recombinant proteins. **Why Other Options are Incorrect:** * **Distribution & Absorption:** These are pharmacokinetic terms. While an adjuvant affects how an antigen is presented locally, its goal is not systemic distribution; in fact, localized retention (depot effect) is often preferred. * **Metabolism:** Adjuvants do not aim to alter the metabolic breakdown of the antigen, but rather its recognition by the immune system. **High-Yield Clinical Pearls for NEET-PG:** * **Alum (Aluminum salts):** The most commonly used adjuvant in human vaccines (e.g., DPT, Hepatitis B). It primarily stimulates a **Th2 response**. * **Freund’s Complete Adjuvant (FCA):** Contains killed *Mycobacteria*; it is highly potent but too toxic for human use (causes granulomas). It is used only in experimental animals. * **Freund’s Incomplete Adjuvant (FIA):** Similar to FCA but lacks the Mycobacteria. * **Newer Adjuvants:** **AS04** (used in HPV vaccines) contains Alum plus MPL (a TLR4 agonist).

Q: Type V hypersensitivity is a type of:

Type II hypersensitivity. ### Explanation **Correct Answer: B. Type II hypersensitivity** **Mechanism:** Type V hypersensitivity is considered a **subtype of Type II hypersensitivity** (Antibody-mediated cytotoxicity). While standard Type II involves antibodies (IgG or IgM) causing cell destruction or inflammation, Type V is specifically characterized by **stimulatory antibodies**. These antibodies bind to cell surface receptors and mimic the natural ligand, leading to continuous activation of the cell rather than its destruction. **Why Type II is correct:** The Gell and Coombs classification originally described four types. Type V was later added to describe "Stimulatory Hypersensitivity." Since it involves antibodies directed against specific cell-surface antigens (receptors), it is functionally a modification of the Type II mechanism. **Why other options are incorrect:** * **Type I:** Mediated by IgE and mast cell degranulation (e.g., Anaphylaxis, Atopy). * **Type III:** Mediated by the deposition of soluble Antigen-Antibody (Immune) complexes in tissues (e.g., SLE, Post-streptococcal glomerulonephritis). * **Type IV:** A delayed-type hypersensitivity mediated by T-cells, not antibodies (e.g., Mantoux test, Contact dermatitis). **Clinical Pearls for NEET-PG:** * **Classic Example:** **Graves’ Disease**, where Long-Acting Thyroid Stimulators (LATS/TSH-receptor antibodies) stimulate the thyroid gland to produce excess T3/T4. * **Another Example:** **Myasthenia Gravis** (though usually inhibitory, it involves antibodies against ACh receptors). * **Key Distinction:** Unlike other Type II reactions, Type V does **not** involve complement activation or cell lysis.

Q: What is true about type II hypersensitivity reactions?

May be complement mediated. **Explanation:** Type II hypersensitivity, also known as **Cytotoxic Hypersensitivity**, occurs when IgG or IgM antibodies bind to antigens on the surface of specific cells or tissues. **Why Option A is Correct:** The binding of IgG or IgM to the cell surface activates the **Classical Complement Pathway**. This leads to the formation of the Membrane Attack Complex (MAC), causing direct cell lysis. Additionally, complement fragments like C3b act as opsonins, facilitating phagocytosis by macrophages. Examples include Autoimmune Hemolytic Anemia and Rh incompatibility. **Why Incorrect Options are Wrong:** * **Option B:** The **Schultz-Dale phenomenon** is a laboratory demonstration of smooth muscle contraction in response to a specific antigen in a sensitized animal; it is a classic feature of **Type I (Immediate) Hypersensitivity**, not Type II. * **Option C:** Type II reactions are strictly **Antibody-Dependent** (IgG and IgM). Antibody-independent reactions are characteristic of Type IV (Cell-mediated) hypersensitivity. * **Option D:** **IgE** is the primary mediator of Type I hypersensitivity (Allergy/Anaphylaxis). Type II involves IgG and IgM. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanisms of Type II:** 1. Complement-mediated lysis, 2. Antibody-dependent cell-mediated cytotoxicity (ADCC) via NK cells, 3. Anti-receptor activity (e.g., Myasthenia Gravis, Graves' disease). * **Direct Coombs Test:** Used to detect Type II reactions on RBC surfaces. * **Mnemonic:** Remember **ACID** (Type I: **A**naphylactic; Type II: **C**ytotoxic; Type III: **I**mmune Complex; Type IV: **D**elayed).

Q: Hyperacute graft rejection is a manifestation of which type of hypersensitivity?

Type II hypersensitivity. **Explanation:** **Hyperacute rejection** occurs within minutes to hours after transplantation. It is a classic example of **Type II (Antibody-mediated) Hypersensitivity**. * **Mechanism:** It is mediated by **pre-formed cytotoxic antibodies** (IgG or IgM) in the recipient’s serum that react against antigens on the donor vascular endothelium. These antibodies are usually directed against ABO blood group antigens or HLA Class I antigens. * **Pathophysiology:** The binding of these antibodies triggers the **complement cascade**, leading to endothelial damage, platelet aggregation, and diffuse intravascular coagulation. This results in rapid thrombosis and ischemic necrosis of the graft (classically described as a "shrunken, purple kidney" on the operating table). **Why other options are incorrect:** * **Type I (Immediate):** Mediated by IgE and mast cell degranulation (e.g., Anaphylaxis, Asthma). It is not involved in graft rejection. * **Type III (Immune-complex):** Involves deposition of antigen-antibody complexes in tissues (e.g., SLE, Serum Sickness). While some chronic rejection components involve complexes, hyperacute rejection is a direct cytotoxic attack. * **Type IV (Delayed-type):** Mediated by T-cells. This is the mechanism behind **Acute Rejection** (days to weeks) and **Chronic Rejection** (months to years), but not hyperacute. **High-Yield Clinical Pearls for NEET-PG:** * **Prevention:** Hyperacute rejection is prevented by **cross-matching** (testing recipient serum against donor lymphocytes). * **Histology:** Characterized by neutrophilic infiltration of arterioles and fibrinoid necrosis. * **Treatment:** There is no effective treatment once it begins; the graft must be removed immediately. * **Common Scenarios:** Usually seen in patients with prior blood transfusions, multiple pregnancies, or previous transplants (sensitization).

Question 1

Which component of the complement system has cell lytic property?

Accepted Answer

Membrane Attack Complex (MAC)

Answer

C3b

Answer

C3a

Answer

C5a

Question 2

Toll-like receptors are present in which of the following cell types?

Accepted Answer

Leukocytes

Answer

Polymorphonuclear leukocytes (PMNs)

Answer

Reticulocytes

Answer

Reticulocytes

Question 3

What is true about the secondary immune response?

Accepted Answer

It is usually of low titre.

Answer

It has a long latent period.

Answer

Antibodies appear in a short time.

Answer

It persists for a long time.

Question 4

Humoral immunodeficiency is suspected in a patient and is under investigation. Which of the following infections would not be consistent with the diagnosis?

Accepted Answer

Pneumocystis jirovecii pneumonia

Answer

Giardiasis

Answer

Recurrent sinusitis

Answer

Recurrent subcutaneous abscesses

Question 5

What is the primary aim of an adjuvant?

Accepted Answer

Antigenicity

Answer

Distribution

Answer

Absorption

Answer

Metabolism

Question 6

Type V hypersensitivity is a type of:

Accepted Answer

Type II hypersensitivity

Answer

Type I hypersensitivity

Answer

Type III hypersensitivity

Answer

Type IV hypersensitivity

Question 7

Skin transplant was done from sister to brother. After a few years, a skin transplant from brother to sister was done, but rejection occurred. This phenomenon is known as?

Accepted Answer

Eichwald-Silmser effect

Answer

Schultz-Dale phenomenon

Answer

Theobald Smith phenomenon

Answer

Shwartzman reaction

Question 8

What is true about type II hypersensitivity reactions?

Accepted Answer

May be complement mediated

Answer

The Schultz-Dale phenomenon is a type II hypersensitivity reaction

Answer

Antibody independent

Answer

Involves IgE

Question 9

Which type of T-lymphocyte is primarily responsible for the histocompatibility reaction?

Accepted Answer

Helper T-cell

Answer

Suppressor T-cell

Answer

Activator T-cell

Answer

Effector T-cell

Question 10

Hyperacute graft rejection is a manifestation of which type of hypersensitivity?

Accepted Answer

Type II hypersensitivity

Answer

Type I hypersensitivity

Answer

Type III hypersensitivity

Answer

Type IV hypersensitivity

Immunology — MCQs

Immunology — MCQs

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