Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 511: Which component of the complement system has cell lytic property?

A. Membrane Attack Complex (MAC) (Correct Answer)
B. C3b
C. C3a
D. C5a

Explanation: **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)."

Question 512: Toll-like receptors are present in which of the following cell types?

A. Polymorphonuclear leukocytes (PMNs)
B. Reticulocytes
C. Reticulocytes
D. Leukocytes (Correct Answer)

Explanation: **Explanation:** **Toll-like Receptors (TLRs)** are a class of Pattern Recognition Receptors (PRRs) that play a crucial role in the **innate immune system**. They recognize highly conserved structural motifs known as Pathogen-Associated Molecular Patterns (PAMPs) found on microbes (e.g., LPS, flagellin, viral RNA). **Why the Correct Answer is Right:** **Leukocytes (Option D)** is the most comprehensive and correct answer. TLRs are primarily expressed on various white blood cells, including **macrophages, dendritic cells, neutrophils (PMNs), B-lymphocytes, and monocytes**. While they are also found on non-immune cells like vascular endothelial cells and mucosal epithelial cells, their highest density and functional significance lie within the leukocyte population to initiate the inflammatory cascade and bridge innate and adaptive immunity. **Analysis of Incorrect Options:** * **Polymorphonuclear leukocytes (PMNs) (Option A):** While PMNs (neutrophils) do express TLRs, this option is too narrow. Since TLRs are found on multiple types of white blood cells (monocytes, DCs, etc.), "Leukocytes" is a more inclusive and accurate choice for a "best fit" answer. * **Reticulocytes (Options B & C):** Reticulocytes are immature red blood cells. They do not possess the immunological machinery or the specific PRRs like TLRs required for pathogen recognition and cytokine signaling. **NEET-PG High-Yield Pearls:** * **Location:** TLRs can be **extracellular** (TLR 1, 2, 4, 5, 6—detecting surface components like LPS) or **intracellular/endosomal** (TLR 3, 7, 8, 9—detecting nucleic acids). * **Specific Ligands:** * **TLR4:** Recognizes Lipopolysaccharide (LPS) of Gram-negative bacteria. * **TLR5:** Recognizes Flagellin. * **TLR3:** Recognizes dsRNA (viral). * **TLR9:** Recognizes unmethylated CpG DNA. * **Signaling:** Most TLRs signal through the **MyD88 pathway**, leading to the activation of **NF-κB**, which triggers the production of pro-inflammatory cytokines.

Question 513: What is true about the secondary immune response?

A. It has a long latent period.
B. It is usually of low titre. (Correct Answer)
C. Antibodies appear in a short time.
D. It persists for a long time.

Explanation: 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.

Question 514: Humoral immunodeficiency is suspected in a patient and is under investigation. Which of the following infections would not be consistent with the diagnosis?

A. Giardiasis
B. Pneumocystis jirovecii pneumonia (Correct Answer)
C. Recurrent sinusitis
D. Recurrent subcutaneous abscesses

Explanation: **Explanation:** The core concept here is distinguishing between **Humoral (B-cell) Immunity** and **Cell-mediated (T-cell) Immunity**. Humoral immunity primarily protects against encapsulated bacteria and certain parasites, while Cell-mediated immunity is essential for controlling intracellular pathogens, fungi, and viruses. **Why Option B is correct:** * ***Pneumocystis jirovecii*** is a fungus that acts as an opportunistic pathogen. Defense against *P. jirovecii* is primarily mediated by **T-cells (CD4+ cells)** and macrophages. * Therefore, *Pneumocystis* pneumonia (PCP) is a hallmark of **T-cell/Cell-mediated immunodeficiency** (e.g., HIV/AIDS, SCID), not isolated humoral immunodeficiency. **Why the other options are wrong:** * **A. Giardiasis:** Secretory IgA is crucial for clearing *Giardia lamblia* from the gut. Patients with Common Variable Immunodeficiency (CVID) or IgA deficiency are highly prone to chronic giardiasis. * **C. Recurrent sinusitis:** Humoral immunity involves B-cells producing antibodies (IgG, IgA) that opsonize encapsulated bacteria like *S. pneumoniae* and *H. influenzae*. Lack of these antibodies leads to recurrent sinopulmonary infections. * **D. Recurrent subcutaneous abscesses:** While often associated with phagocytic defects (like CGD), recurrent pyogenic skin infections are also common in B-cell defects (e.g., X-linked Agammaglobulinemia) due to the inability to opsonize *Staphylococcus aureus*. **High-Yield Clinical Pearls for NEET-PG:** 1. **B-cell defects:** Present after 6 months of age (once maternal IgG wanes) with recurrent infections by **encapsulated bacteria** (*S. pneumoniae, H. influenzae, N. meningitidis*). 2. **T-cell defects:** Present early in infancy with **opportunistic infections** (Fungi like *Candida*, *Pneumocystis*; Viruses like CMV; and Mycobacteria). 3. **Selective IgA Deficiency:** The most common primary immunodeficiency; often presents with respiratory/GI infections or anaphylaxis during blood transfusions.

Question 515: What is the primary aim of an adjuvant?

A. Distribution
B. Absorption
C. Antigenicity (Correct Answer)
D. Metabolism

Explanation: **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).

Question 516: Type V hypersensitivity is a type of:

A. Type I hypersensitivity
B. Type II hypersensitivity (Correct Answer)
C. Type III hypersensitivity
D. Type IV hypersensitivity

Explanation: ### 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.

Question 517: 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?

A. Eichwald-Silmser effect (Correct Answer)
B. Schultz-Dale phenomenon
C. Theobald Smith phenomenon
D. Shwartzman reaction

Explanation: ### Explanation **1. Why Option A is Correct: Eichwald-Silmser Effect** The **Eichwald-Silmser effect** refers to the immunological rejection of male tissue by a female recipient of the same inbred strain. This occurs because males possess the **H-Y antigen**, a minor histocompatibility antigen encoded on the Y chromosome. * **In this scenario:** When the sister (XX) donated to the brother (XY), no rejection occurred because the sister lacks Y-linked antigens. However, when the brother (XY) donated to the sister (XX), her immune system recognized the H-Y antigen as "foreign," leading to graft rejection. **2. Why Other Options are Incorrect** * **B. Schultz-Dale Phenomenon:** An *in vitro* laboratory method used to demonstrate immediate (Type I) hypersensitivity. It involves the contraction of isolated smooth muscle (e.g., guinea pig ileum) when exposed to a specific antigen to which it was previously sensitized. * **C. Theobald Smith Phenomenon:** An older term for **experimental systemic anaphylaxis**. It describes the fatal reaction seen in guinea pigs when they are injected with a second, "challenging" dose of an antigen after an initial sensitizing dose. * **D. Shwartzman Reaction:** A non-immunological phenomenon of localized or systemic tissue necrosis (usually in the kidneys) following two sequential injections of bacterial endotoxins (LPS). It is not related to transplant rejection. **3. High-Yield Clinical Pearls for NEET-PG** * **H-Y Antigen:** It is a **minor histocompatibility antigen**. While HLA (Major) mismatch causes rapid rejection, minor antigens like H-Y can cause rejection even in HLA-matched siblings. * **Laws of Transplantation:** Grafts between identical twins (Isografts) are accepted; grafts between different species (Xenografts) are rejected; grafts from male to female in the same strain may be rejected due to the Eichwald-Silmser effect. * **Memory Tip:** Remember **"Male to Female = Fail"** (due to the Y chromosome).

Question 518: What is true about type II hypersensitivity reactions?

A. May be complement mediated (Correct Answer)
B. The Schultz-Dale phenomenon is a type II hypersensitivity reaction
C. Antibody independent
D. Involves IgE

Explanation: **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).

Question 519: Which type of T-lymphocyte is primarily responsible for the histocompatibility reaction?

A. Suppressor T-cell
B. Activator T-cell
C. Effector T-cell
D. Helper T-cell (Correct Answer)

Explanation: **Explanation:** The **Helper T-cell (CD4+ T-cell)** is the central orchestrator of the immune response, including the histocompatibility (graft rejection) reaction. When a foreign tissue is transplanted, its Major Histocompatibility Complex (MHC) molecules are recognized by the recipient’s Helper T-cells. Once activated, these cells secrete cytokines (like IL-2 and IFN-γ) that trigger a cascade: they activate Cytotoxic T-cells (CD8+) for direct cell lysis, stimulate B-cells to produce antibodies, and recruit macrophages for delayed-type hypersensitivity. Without the initial recognition and signaling by Helper T-cells, the full-scale histocompatibility reaction cannot be sustained. **Analysis of Incorrect Options:** * **A. Suppressor T-cell (Regulatory T-cells):** These cells function to *dampen* the immune response and maintain self-tolerance. They inhibit rather than initiate the histocompatibility reaction. * **B. Activator T-cell:** This is a general functional description rather than a specific biological subset of T-lymphocytes recognized in standard immunology nomenclature for this reaction. * **C. Effector T-cell:** While Cytotoxic T-cells (a type of effector cell) perform the actual "killing" of the graft, the *primary responsibility* for initiating and coordinating the rejection process lies with the Helper T-cell. **High-Yield Clinical Pearls for NEET-PG:** * **MHC Restriction:** CD4+ Helper T-cells recognize antigens presented with **MHC Class II**, while CD8+ Cytotoxic T-cells recognize **MHC Class I**. * **Direct vs. Indirect Recognition:** In direct recognition, recipient T-cells react to intact donor MHC; in indirect recognition, recipient T-cells react to donor peptides presented by recipient APCs. * **Hyperacute Rejection:** Occurs within minutes due to pre-formed antibodies (Type II Hypersensitivity). * **Acute Rejection:** Primarily T-cell mediated (Type IV Hypersensitivity), where Helper T-cells play the pivotal role.

Question 520: Hyperacute graft rejection is a manifestation of which type of hypersensitivity?

A. Type I hypersensitivity
B. Type II hypersensitivity (Correct Answer)
C. Type III hypersensitivity
D. Type IV hypersensitivity

Explanation: **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).

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Complement System

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Cytokines and Chemokines

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Hypersensitivity Reactions

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Immunology — MCQs

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