generate most important high yield MCQs for batterjee medical college exams as i have less time to review so generate absolute must know MCQs with pictures/diagram
Reading File
Running Command
cd /home/daytona/workspace/attachments/0cc19f0c-7b2e-4f05-9ee2-b94e4f7dc6ac && p…
Searching Images
complement activation pathways classical alternative lectin diagram
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antibody immunoglobulin structure Fab Fc heavy light chain
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T helper cell subsets Th1 Th2 Th17 cytokines functions
Searching Images
cytotoxic T cell killing mechanism perforin granzyme
Reading File
Running Command
mkdir -p /home/daytona/workspace/immunology-mcqs
Writing File
~/immunology-mcqs/immunology_mcqs.html
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<title>Immunology High-Yield MCQs – Batterjee Medical College</title>
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<div class="cover">
<h1>🧬 Immunology High-Yield MCQs</h1>
<h2>Batterjee Medical College · Microbiology Department</h2>
<div class="badge">L1: Innate Immunity</div>
<div class="badge">L2: Complement Activation</div>
<div class="badge">L3: Humoral Immunity</div>
<div class="badge">L4: Cell-Mediated Immunity</div>
<p style="margin-top:22px; opacity:0.75; font-size:0.9em;">30 Must-Know MCQs with Explanations & Visual Aids</p>
</div>
<!-- TABLE OF CONTENTS -->
<div class="toc">
<h2>📋 Topics Covered</h2>
<ul>
<li><a href="#l1">• Innate vs Adaptive Immunity</a></li>
<li><a href="#l1">• PAMPs & PRRs / TLRs</a></li>
<li><a href="#l1">• Natural Barriers (Defensins, CF)</a></li>
<li><a href="#l1">• Acute Phase Response / CRP</a></li>
<li><a href="#l1">• Cells: Neutrophils, NK, Macrophages</a></li>
<li><a href="#l2">• Complement Pathways</a></li>
<li><a href="#l2">• C3, C5a, MAC Functions</a></li>
<li><a href="#l2">• Complement Regulation & DAF/CD59</a></li>
<li><a href="#l2">• Clinical: HAE, PNH, Neisseria</a></li>
<li><a href="#l3">• Antigen, Hapten, Adjuvant</a></li>
<li><a href="#l3">• Antibody Structure (Fab/Fc/Papain)</a></li>
<li><a href="#l3">• Immunoglobulin Classes & Functions</a></li>
<li><a href="#l3">• Primary vs Secondary Response</a></li>
<li><a href="#l4">• T Cell Subsets (CD4/CD8)</a></li>
<li><a href="#l4">• Th1/Th2/Th17/Treg Cytokines</a></li>
<li><a href="#l4">• Active vs Passive Immunity</a></li>
<li><a href="#l4">• Cytotoxic T Cell Mechanisms</a></li>
</ul>
</div>
<!-- ======================================================= -->
<!-- SECTION 1: INNATE IMMUNITY -->
<!-- ======================================================= -->
<div class="section-header" id="l1">🛡️ Section 1: Innate Immunity <span>(L1 — 8 MCQs)</span></div>
<div class="mcq-container">
<!-- Q1 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">1</div>
<div class="q-text">Which of the following is a feature of INNATE immunity that distinguishes it from adaptive immunity?</div>
</div>
<div class="options">
<div class="option wrong">A. Generates immunological memory</div>
<div class="option wrong">B. Involves somatic recombination of gene segments</div>
<div class="option correct">C. Responds immediately without prior antigen exposure</div>
<div class="option wrong">D. Recognizes unique epitopes on specific antigens</div>
<div class="option wrong">E. Produces antibodies</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p>Innate immunity is <strong>pre-formed, rapid (minutes to hours)</strong>, and uses germline-encoded PRRs recognizing PAMPs — broad patterns shared by classes of microbes. It has <strong>no immunological memory</strong>. Adaptive immunity uses somatic recombination to generate diverse, antigen-specific receptors (>10⁷ specificities) and does generate memory.</p>
</div>
<div class="key-fact">🔑 Key: Innate = fast, nonspecific, no memory | Adaptive = slow, specific, memory</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q2 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">2</div>
<div class="q-text">Which of the following is the BEST example of a PAMP (Pathogen-Associated Molecular Pattern)?</div>
</div>
<div class="options">
<div class="option wrong">A. Human glycoproteins</div>
<div class="option wrong">B. Host DNA</div>
<div class="option correct">C. Lipopolysaccharide (LPS)</div>
<div class="option wrong">D. Human albumin</div>
<div class="option wrong">E. Fibronectin</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p>PAMPs are molecular structures <strong>found on microbes but absent from normal human cells</strong>. Classic examples include: <strong>LPS</strong> (gram-negative bacterial cell wall), <strong>peptidoglycan</strong>, and <strong>double-stranded RNA</strong>. They are essential for microbial survival, so microbes cannot easily mutate them. PAMPs are recognized by PRRs (e.g., TLRs) on innate immune cells.</p>
</div>
<div class="key-fact">🔑 PAMPs: LPS, Peptidoglycan, dsRNA — recognized by TLRs, NLRs, RLRs, CLRs</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q3 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">3</div>
<div class="q-text">A patient with cystic fibrosis (CF) suffers from recurrent pulmonary infections with Pseudomonas aeruginosa. Which barrier dysfunction is primarily responsible?</div>
</div>
<div class="options">
<div class="option wrong">A. Loss of skin integrity</div>
<div class="option wrong">B. Deficiency of defensins</div>
<div class="option correct">C. Impaired mucociliary escalator due to thick mucus</div>
<div class="option wrong">D. Reduced gastric acid secretion</div>
<div class="option wrong">E. Depletion of commensal bacteria</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p>In CF, the CFTR mutation causes <strong>abnormally thick, viscous mucus</strong> that the cilia cannot move effectively — the <strong>mucociliary escalator fails</strong>. This allows bacteria like <strong>Pseudomonas aeruginosa</strong> to colonize and cause chronic lung infections. Normal mucus traps microbes; cilia beat them out of the airways.</p>
</div>
<span class="tag clinical">Clinical</span><span class="tag high">High Yield</span>
</div>
<!-- Q4 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">4</div>
<div class="q-text">After antibiotic therapy, a patient develops pseudomembranous colitis. The causative organism is Clostridium difficile. What is the mechanism?</div>
</div>
<div class="options">
<div class="option wrong">A. C. difficile was introduced by the antibiotics</div>
<div class="option wrong">B. Antibiotics suppressed neutrophil activity</div>
<div class="option correct">C. Antibiotics disrupted normal flora, allowing C. difficile overgrowth</div>
<div class="option wrong">D. Antibiotics caused direct intestinal mucosal injury</div>
<div class="option wrong">E. Complement was activated by antibiotic-antigen complexes</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p>Commensal (normal) bacteria protect against pathogens via <strong>competition for nutrients</strong> and <strong>production of bacteriocins</strong>. Broad-spectrum antibiotics <strong>reduce normal flora</strong>, removing this biological barrier. <strong>C. difficile</strong> (which is resistant or present in low numbers) then <strong>overgrows</strong> and produces toxins, causing pseudomembranous colitis.</p>
</div>
<div class="key-fact">🔑 Commensal flora = biological barrier. Disruption → C. difficile overgrowth</div>
<span class="tag clinical">Clinical</span><span class="tag high">High Yield</span>
</div>
<!-- Q5 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">5</div>
<div class="q-text">Which antimicrobial peptide creates pores in bacterial cell membranes and is produced by neutrophils and Paneth cells (α-type) and epithelial cells (β-type)?</div>
</div>
<div class="options">
<div class="option wrong">A. Lysozyme</div>
<div class="option correct">B. Defensins</div>
<div class="option wrong">C. Cathelicidins (different class)</div>
<div class="option wrong">D. Histamine</div>
<div class="option wrong">E. Myeloperoxidase</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p><strong>Defensins</strong> are <strong>cationic peptides</strong> that disrupt bacterial membrane integrity by forming pores. <strong>α-defensins</strong>: produced by neutrophils and <strong>Paneth cells</strong> (intestinal crypts). <strong>β-defensins</strong>: produced by <strong>epithelial cells</strong> of skin and mucous membranes. Lysozyme breaks peptidoglycan but doesn't form pores.</p>
</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q6 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">6</div>
<div class="q-text">C-Reactive Protein (CRP) exerts its protective effects primarily by which mechanism?</div>
</div>
<div class="options">
<div class="option wrong">A. Directly killing bacteria via pore formation</div>
<div class="option wrong">B. Inhibiting complement activation</div>
<div class="option correct">C. Binding phosphorylcholine on bacterial walls → activates complement + acts as opsonin</div>
<div class="option wrong">D. Stimulating mast cell degranulation</div>
<div class="option wrong">E. Acting as a chemotactic factor for eosinophils</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p>CRP binds <strong>phosphorylcholine</strong> (on bacterial cell wall phospholipids). This activates the <strong>classical complement pathway</strong> AND enhances <strong>opsonization</strong> (phagocytosis). CRP levels increase <strong>up to 1000-fold</strong> in infection/inflammation, making it a sensitive non-specific biomarker. Key mediators of the Acute Phase Response: <strong>IL-1, IL-6, TNF-α</strong>.</p>
</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q7 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">7</div>
<div class="q-text">Which of the following leukocytes is the MOST NUMEROUS in peripheral blood and is the primary cell responsible for phagocytosis of bacteria during acute infection?</div>
</div>
<div class="options">
<div class="option wrong">A. Monocyte</div>
<div class="option wrong">B. Eosinophil</div>
<div class="option wrong">C. Natural killer cell</div>
<div class="option correct">D. Neutrophil (PMN)</div>
<div class="option wrong">E. Basophil</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p>Neutrophils = <strong>60% of peripheral blood leukocytes</strong>. They are <strong>polymorphonuclear (PMN)</strong> (3–5 nuclear segments), have cytoplasmic granules with <strong>myeloperoxidase</strong> (responsible for the yellowish-green color of pus), and have a short lifespan. Decreased neutrophils (neutropenia) → predisposes to <strong>bacterial infections</strong>.</p>
</div>
<div class="key-fact">🔑 Neutrophil facts: Most numerous | PMN | Myeloperoxidase = yellow-green pus | Neutropenia → bacterial infections</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q8 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">8</div>
<div class="q-text">IL-8 is primarily produced at sites of infection by macrophages and epithelial cells. What is its PRIMARY function?</div>
</div>
<div class="options">
<div class="option wrong">A. Activating natural killer cells</div>
<div class="option wrong">B. Inducing fever</div>
<div class="option wrong">C. Opsonizing bacteria</div>
<div class="option correct">D. Chemotactic recruitment of neutrophils (granulocytes) to the infection site</div>
<div class="option wrong">E. Stimulating IgE production</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p><strong>IL-8</strong> is the <strong>main chemotactic factor for granulocytes</strong> (neutrophils, basophils, eosinophils) and is the key component of <strong>pus/abscess formation</strong>. Produced by epithelial cells, endothelial cells, smooth muscle cells, and macrophages at infection sites. Compare: <strong>C5a</strong> is the most potent chemotactic factor from the complement system for neutrophils.</p>
</div>
<span class="tag high">High Yield</span>
</div>
</div><!-- end section 1 -->
<!-- ======================================================= -->
<!-- SECTION 2: COMPLEMENT ACTIVATION -->
<!-- ======================================================= -->
<div class="section-header" id="l2">⚗️ Section 2: Complement Activation <span>(L2 — 8 MCQs)</span></div>
<div class="mcq-container">
<!-- Complement Diagram -->
<div class="mcq-card" style="border-left-color: #6a1b9a;">
<div class="image-box">
<img src="https://cdn.orris.care/cdss_images/pmc_clinical_VQA_d2fa6eaef65ba9db3932aef137c6ed843ac0b63298964c4ec0acf211ac1eb4d3.jpg" alt="Complement Activation Pathways Diagram">
<div class="caption">Fig 1. Three pathways of complement activation converging at C3, leading to MAC formation and inflammatory mediators (C3a, C5a). Note amplification loop and regulatory factors (Factor I/H, CD59).</div>
</div>
</div>
<!-- Q9 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">9</div>
<div class="q-text">Which complement pathway is activated by IgM or IgG antibodies bound to antigen?</div>
</div>
<div class="options">
<div class="option correct">A. Classical pathway</div>
<div class="option wrong">B. Alternative pathway</div>
<div class="option wrong">C. Lectin (MBL) pathway</div>
<div class="option wrong">D. All three equally</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p>The <strong>Classical pathway</strong> is activated when <strong>C1q binds to the Fc region of IgG or IgM</strong> (mainly IgG1, IgG3, or IgM) in antigen-antibody complexes. <strong>IgM is more efficient</strong> (pentameric — provides multiple C1q binding sites). The <strong>Alternative pathway</strong> activates without antibody (spontaneous C3 hydrolysis + Factor B/D/Properdin). The <strong>Lectin pathway</strong> uses MBL/ficolins binding to mannose residues on pathogens + MASPs.</p>
</div>
<div class="key-fact">🔑 Classical = Antibody (IgG/IgM) | Alternative = No antibody, Factor B/D/Properdin | Lectin = MBL + MASP</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q10 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">10</div>
<div class="q-text">C3 convertase in the CLASSICAL pathway is composed of which fragments?</div>
</div>
<div class="options">
<div class="option wrong">A. C3b + Bb</div>
<div class="option correct">B. C4b + C2b</div>
<div class="option wrong">C. C1q + C1r + C1s</div>
<div class="option wrong">D. C5b + C6</div>
<div class="option wrong">E. C3b + C4b</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p>In the Classical pathway: C1 activates → cleaves C2 and C4 → <strong>C4b + C2b</strong> bind on the bacterial surface to form the <strong>C3 convertase (C4b2b)</strong>. This then cleaves C3 → C3a + C3b. In the <strong>Alternative pathway</strong> the C3 convertase is <strong>C3bBb</strong> (stabilized by Properdin). Both ultimately produce C3b for opsonization and MAC formation.</p>
</div>
<div class="key-fact">🔑 Classical C3 convertase = C4b2b | Alternative C3 convertase = C3bBb (+ Properdin)</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q11 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">11</div>
<div class="q-text">Which complement fragment is the MOST POTENT chemotactic factor for leukocytes?</div>
</div>
<div class="options">
<div class="option wrong">A. C3a</div>
<div class="option wrong">B. C3b</div>
<div class="option correct">C. C5a</div>
<div class="option wrong">D. C4a</div>
<div class="option wrong">E. C5b</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p><strong>C5a</strong> is the <strong>most powerful chemotactic factor</strong> for leukocytes (especially neutrophils). It also enhances neutrophil adhesiveness to endothelium and causes mast cell degranulation (histamine release). <strong>C3a and C4a</strong> are also anaphylatoxins (mast cell degranulation) but are weaker chemotactic agents. <strong>C3b</strong> is the key opsonin. <strong>C5b</strong> initiates MAC formation.</p>
</div>
<div class="key-fact">🔑 Anaphylatoxins (mast cell degranulation): C3a, C4a, C5a | Chemotaxis (most potent): C5a | Opsonin: C3b</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q12 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">12</div>
<div class="q-text">The Membrane Attack Complex (MAC) is composed of which complement components?</div>
</div>
<div class="options">
<div class="option wrong">A. C1, C2, C3</div>
<div class="option wrong">B. C3b, C4b, C2b</div>
<div class="option correct">C. C5b, C6, C7, C8, C9</div>
<div class="option wrong">D. C3b + Factor B + Properdin</div>
<div class="option wrong">E. C1q, C1r, C1s</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p>The MAC (C5b-9) forms a <strong>transmembrane pore</strong> in the bacterial/target cell membrane. Sequence: <strong>C5b → binds C6 → C7 → C8 → multiple C9 molecules polymerize</strong> to form the ring-shaped pore. This allows cytoplasm to leak out, water to rush in → <strong>osmotic lysis</strong>. MAC is especially important against <strong>Neisseria species</strong>.</p>
</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q13 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">13</div>
<div class="q-text">A patient presents with recurrent Neisseria meningitidis infections. Which complement deficiency is most likely?</div>
</div>
<div class="options">
<div class="option wrong">A. C1 deficiency</div>
<div class="option wrong">B. C3 deficiency</div>
<div class="option correct">C. C5–C9 deficiency (terminal complement)</div>
<div class="option wrong">D. Factor B deficiency</div>
<div class="option wrong">E. MBL deficiency</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p>Deficiency of <strong>C5–C9</strong> (terminal complement components forming the MAC) leads to susceptibility to <strong>Neisseria</strong> infections (N. meningitidis, N. gonorrhoeae) because MAC is the primary mechanism of killing encapsulated gram-negative diplococci. <strong>C3 deficiency</strong> → severe pyogenic bacterial infections (sinusitis, respiratory). Liver disease → cannot synthesize complement → pyogenic infections.</p>
</div>
<div class="key-fact">🔑 C3 deficiency → all pyogenic bacteria | C5-C9 deficiency → Neisseria specifically</div>
<span class="tag clinical">Clinical</span><span class="tag high">High Yield</span>
</div>
<!-- Q14 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">14</div>
<div class="q-text">A 40-year-old man presents with recurrent episodes of facial and laryngeal angioedema without urticaria. Which deficiency explains this?</div>
</div>
<div class="options">
<div class="option wrong">A. C3 deficiency</div>
<div class="option wrong">B. C5–C9 deficiency</div>
<div class="option wrong">C. Factor H deficiency</div>
<div class="option correct">D. C1 inhibitor (C1 INH) deficiency → Hereditary Angioedema</div>
<div class="option wrong">E. CD59 deficiency</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p><strong>Hereditary Angioedema (HAE)</strong> is caused by inherited deficiency of <strong>C1 inhibitor (C1 INH)</strong>. Normally, C1 INH inactivates/dissociates C1r-C1s from C1q, preventing excessive classical pathway activation. Without C1 INH, uncontrolled complement activation → accumulation of <strong>bradykinin</strong> → vascular permeability → <strong>angioedema</strong> (lips, face, larynx, abdomen). <strong>No urticaria</strong> distinguishes HAE from allergic angioedema.</p>
</div>
<div class="key-fact">🔑 HAE = C1 INH deficiency | PNH = DAF (CD55) deficiency → hemolysis</div>
<span class="tag clinical">Clinical</span><span class="tag high">High Yield</span>
</div>
<!-- Q15 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">15</div>
<div class="q-text">Paroxysmal nocturnal hemoglobinuria (PNH) results from acquired deficiency of which complement regulatory protein?</div>
</div>
<div class="options">
<div class="option wrong">A. C1 inhibitor</div>
<div class="option correct">B. Decay-accelerating factor (DAF / CD55)</div>
<div class="option wrong">C. Factor H</div>
<div class="option wrong">D. Properdin</div>
<div class="option wrong">E. MASP-2</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p><strong>DAF (CD55)</strong> normally displaces C2b from C4b and Bb from C3b (dissociates C3 convertases), protecting host cells from complement. <strong>CD59 (Protectin)</strong> inhibits MAC formation. In PNH, a somatic mutation in <strong>PIG-A gene</strong> → lack of GPI anchor → absence of DAF and CD59 on red blood cells → complement attacks patient's own RBCs → <strong>intravascular hemolysis</strong>, dark morning urine.</p>
</div>
<div class="key-fact">🔑 PNH: DAF (CD55) + CD59 both missing → RBC hemolysis | HAE: C1 INH missing → angioedema</div>
<span class="tag clinical">Clinical</span><span class="tag high">High Yield</span>
</div>
<!-- Q16 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">16</div>
<div class="q-text">In a patient with acute post-streptococcal glomerulonephritis, serum complement levels are LOW. Why?</div>
</div>
<div class="options">
<div class="option wrong">A. The kidneys stop producing complement</div>
<div class="option wrong">B. Complement is destroyed by streptococcal enzymes</div>
<div class="option correct">C. Complement is consumed by immune complex deposition</div>
<div class="option wrong">D. Complement activation is inhibited by antibodies</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p>In <strong>immune complex diseases</strong> (e.g., post-streptococcal GN, SLE, serum sickness), <strong>antigen-antibody complexes activate complement</strong>, consuming it. The resulting low complement levels (especially C3, C4) serve as a diagnostic marker. The immune complexes deposit in glomeruli → complement activation → inflammation → glomerulonephritis.</p>
</div>
<span class="tag clinical">Clinical</span>
</div>
</div><!-- end section 2 -->
<!-- ======================================================= -->
<!-- SECTION 3: HUMORAL IMMUNITY -->
<!-- ======================================================= -->
<div class="section-header" id="l3">💉 Section 3: Humoral Immunity <span>(L3 — 7 MCQs)</span></div>
<div class="mcq-container">
<!-- Ab Structure Diagram -->
<div class="mcq-card" style="border-left-color: #2e7d32;">
<div class="image-box">
<img src="https://cdn.orris.care/cdss_images/pmc_clinical_VQA_4ad582149d56513876a7381c9989d4cdcf157f80cb09362d07cbb4f11214292b.jpg" alt="IgG antibody structure diagram">
<div class="caption">Fig 2. IgG antibody structure: Y-shape with two heavy (blue) and two light (orange) chains. Fab region = antigen binding; Fc region = effector functions (complement activation, Fc receptor binding, opsonization).</div>
</div>
</div>
<!-- Q17 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">17</div>
<div class="q-text">Papain cleaves IgG into three fragments. Which fragment is responsible for antigen binding?</div>
</div>
<div class="options">
<div class="option correct">A. Two Fab fragments (Fragment Antigen Binding)</div>
<div class="option wrong">B. One Fc fragment (Fragment Crystallizable)</div>
<div class="option wrong">C. The hinge region</div>
<div class="option wrong">D. The CH2 domain</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p>Papain cleaves IgG into: <strong>2 × Fab fragments</strong> (each contains one VH + VL domain → antigen binding) and <strong>1 × Fc fragment</strong> (no antigen affinity; mediates effector functions: complement fixation, opsonization, placental transport, mast cell binding). The Fc region contains the <strong>constant domains of heavy chains (CH2, CH3)</strong>. The <strong>flexible hinge region</strong> between CH1 and CH2 allows antigen-binding arm movement.</p>
</div>
<div class="key-fact">🔑 Papain: 2 Fab (antigen binding) + 1 Fc (effector) | Pepsin: 1 F(ab')₂ fragment</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q18 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">18</div>
<div class="q-text">Which antibody isotype is the ONLY one that crosses the placenta, providing neonatal protection?</div>
</div>
<div class="options">
<div class="option wrong">A. IgM</div>
<div class="option wrong">B. IgA</div>
<div class="option correct">C. IgG</div>
<div class="option wrong">D. IgE</div>
<div class="option wrong">E. IgD</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p><strong>IgG</strong> is transported across the placenta via the <strong>neonatal Fc receptor (FcRn)</strong> on syncytiotrophoblast cells. It is the <strong>predominant antibody in serum</strong>, mediates opsonization, complement fixation (IgG1, IgG3), ADCC, and neonatal immunity. <strong>IgA</strong> is the main antibody in <strong>secretions (breast milk, saliva, tears)</strong> — passive immunity via breastfeeding. <strong>IgM</strong> is first in primary response; cannot cross placenta (pentamer, too large). <strong>IgE</strong>: allergic reactions, anti-helminth.</p>
</div>
<div class="key-fact">🔑 IgG = crosses placenta | IgA = secretions/breast milk | IgM = first in primary response | IgE = allergy/helminths | IgD = B cell receptor</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q19 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">19</div>
<div class="q-text">A 35-year-old breastfeeding mother has a minor throat infection. Her doctor reassures her the baby is protected via breast milk. Which antibody class is most important in this protection?</div>
</div>
<div class="q-scenario">📋 Case: The antibody present in breast milk prevents attachment of microorganisms to mucosal membranes of the infant's GI and respiratory tracts.</div>
<div class="options">
<div class="option correct">A. IgA (secretory IgA)</div>
<div class="option wrong">B. IgM</div>
<div class="option wrong">C. IgD</div>
<div class="option wrong">D. IgE</div>
<div class="option wrong">E. IgG</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p><strong>Secretory IgA (sIgA)</strong> is the dominant antibody in <strong>breast milk, saliva, tears, and colostrum</strong>. It provides <strong>mucosal immunity</strong> by preventing attachment of bacteria and viruses to mucosal surfaces. It is transported across epithelial cells by the <strong>poly-Ig receptor</strong> and has a secretory component that protects it from proteases. This is passive immunity for the newborn.</p>
</div>
<span class="tag clinical">Clinical</span><span class="tag high">High Yield</span>
</div>
<!-- Q20 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">20</div>
<div class="q-text">In the PRIMARY antibody response, which immunoglobulin class predominates in the LOG phase?</div>
</div>
<div class="options">
<div class="option wrong">A. IgG</div>
<div class="option correct">B. IgM</div>
<div class="option wrong">C. IgA</div>
<div class="option wrong">D. IgE</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p><strong>Primary response</strong>: Lag phase = 7–10 days (generating B cells) → Log phase predominates with <strong>IgM</strong> → Plateau → Decline. <strong>Secondary response</strong>: Short lag (3–5 days, memory B cells) → Predominantly <strong>IgG</strong> → higher quantity, longer duration, higher affinity (<strong>affinity maturation</strong>). The switch from IgM → IgG requires <strong>Tfh (follicular helper T) cell help via CD40L-CD40 interaction</strong> in germinal centers.</p>
</div>
<div class="key-fact">🔑 1° response: IgM first, long lag | 2° response: IgG, short lag, higher titer, affinity maturation</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q21 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">21</div>
<div class="q-text">Which antibody isotype activates complement most EFFICIENTLY and is found as a pentamer?</div>
</div>
<div class="options">
<div class="option wrong">A. IgG</div>
<div class="option correct">B. IgM</div>
<div class="option wrong">C. IgA</div>
<div class="option wrong">D. IgE</div>
<div class="option wrong">E. IgD</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p><strong>IgM</strong> is a <strong>pentamer</strong> (5 monomers linked by J-chain), making it excellent at complement activation via the classical pathway. A single IgM molecule has 10 antigen-binding sites (but only 5 are typically accessible). Its pentameric structure provides <strong>multiple Fc regions for C1q binding</strong>. It is produced first in the primary response (before class switching). Though IgG and IgM both activate complement, <strong>IgM is far more efficient per molecule</strong>.</p>
</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q22 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">22</div>
<div class="q-text">Antibody-Dependent Cell-mediated Cytotoxicity (ADCC) against helminth infections is primarily mediated by which immunoglobulin class binding to eosinophils?</div>
</div>
<div class="options">
<div class="option wrong">A. IgG via FcγR on eosinophils</div>
<div class="option wrong">B. IgM via complement</div>
<div class="option wrong">C. IgA via secretory component</div>
<div class="option correct">D. IgE via FcεR on eosinophils</div>
<div class="option wrong">E. IgD as B cell receptor</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p>In ADCC against helminths: <strong>IgE</strong> coats the parasite → <strong>Fc epsilon receptors on eosinophils</strong> recognize the IgE → eosinophils degranulate releasing <strong>toxic granule proteins</strong> (major basic protein, eosinophil peroxidase) that kill the helminth. NK cells perform ADCC via <strong>FcγR (CD16) recognizing IgG</strong> on virus-infected/tumor cells. Remember: <strong>IL-5</strong> activates eosinophils; <strong>IL-4</strong> increases IgE production (both from Th2 cells).</p>
</div>
<div class="key-fact">🔑 ADCC: NK cell + IgG → virus/tumor | Eosinophil + IgE → helminths</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q23 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">23</div>
<div class="q-text">A hapten is best described as:</div>
</div>
<div class="options">
<div class="option wrong">A. A molecule that stimulates immune response independently</div>
<div class="option correct">B. A low-MW molecule that binds antibodies but cannot elicit an immune response alone</div>
<div class="option wrong">C. A substance that increases immunogenicity when injected with antigen</div>
<div class="option wrong">D. A protein that activates T cells without antigen processing</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p>A <strong>hapten</strong> can be recognized by antibodies (acts as antigen) but cannot stimulate an immune response on its own (not immunogenic). It becomes immunogenic when <strong>conjugated to a carrier protein</strong>. Example: <strong>penicillin</strong> (small molecule) acts as a hapten — it binds to serum proteins, forming a hapten-carrier complex that elicits anti-penicillin antibodies → allergic reactions. An <strong>adjuvant</strong> is different: it enhances immunogenicity of an antigen (e.g., aluminum hydroxide in vaccines).</p>
</div>
<span class="tag high">High Yield</span>
</div>
</div><!-- end section 3 -->
<!-- ======================================================= -->
<!-- SECTION 4: CELL-MEDIATED IMMUNITY -->
<!-- ======================================================= -->
<div class="section-header" id="l4">🔬 Section 4: Cell-Mediated Immunity <span>(L4 — 7 MCQs)</span></div>
<div class="mcq-container">
<!-- Th subset diagram -->
<div class="mcq-card" style="border-left-color: #e65100;">
<div class="image-box">
<img src="https://cdn.orris.care/cdss_images/pmc_clinical_VQA_21554306e83d1b56884a856035cdeacf70e6d67b09101e12672ed73e9c5eb3a2.jpg" alt="CD4+ T helper cell subsets differentiation diagram">
<div class="caption">Fig 3. CD4+ T helper cell differentiation: Naïve CD4+ T cell → Th1 (IL-12/IL-18 → IFN-γ → cell-mediated immunity), Th2 (IL-4 → IL-4/IL-13 → humoral/helminth), Th17 (IL-6+TGF-β → IL-17/IL-22 → mucosal), Treg (TGF-β → IL-10/TGF-β → suppression). Transcription factors: Tbet, GATA-3, RORγt, FoxP3.</div>
</div>
</div>
<!-- Perforin diagram -->
<div class="mcq-card" style="border-left-color: #e65100;">
<div class="image-box">
<img src="https://cdn.orris.care/cdss_images/pmc_clinical_VQA_b1ee4444e724676c58a311a0c6974d72bcab00d8e2d02111afd2d42ebff581af.jpg" alt="Cytotoxic T cell perforin granzyme killing mechanism">
<div class="caption">Fig 4. CTL killing: Perforin monomers oligomerize → transmembrane pore → Granzymes enter target cell → apoptosis. Also FasL-Fas interaction triggers apoptosis.</div>
</div>
</div>
<!-- Q24 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">24</div>
<div class="q-text">CD4+ T helper cells recognize antigen presented on which MHC molecule?</div>
</div>
<div class="options">
<div class="option wrong">A. MHC class I on all nucleated cells</div>
<div class="option correct">B. MHC class II on antigen-presenting cells (APCs)</div>
<div class="option wrong">C. MHC class I on red blood cells</div>
<div class="option wrong">D. MHC class II on cytotoxic T cells</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p><strong>CD4+ (Helper) T cells</strong> recognize peptide on <strong>MHC class II</strong> (expressed by APCs: macrophages, dendritic cells, B cells) → <strong>MHC II restricted</strong>. <strong>CD8+ (Cytotoxic) T cells</strong> recognize peptide on <strong>MHC class I</strong> (expressed on ALL nucleated cells) → <strong>MHC I restricted</strong>. Key rule: <strong>CD4 binds MHC II | CD8 binds MHC I</strong>.</p>
</div>
<div class="key-fact">🔑 CD4 = MHC II = helper = orchestrates response | CD8 = MHC I = cytotoxic = kills infected cells</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q25 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">25</div>
<div class="q-text">A patient develops granulomatous inflammation in the lung (histology shows epithelioid macrophages surrounded by lymphocytes). Which T helper subset is primarily responsible?</div>
</div>
<div class="q-scenario">📋 Case: 35-year-old male, returned from Pakistan 5 months ago. Productive cough, weight loss, hilar lymphadenopathy, pleural effusion. Lung biopsy shows granuloma.</div>
<div class="options">
<div class="option correct">A. Th1 cells (secrete IFN-γ → macrophage activation → granuloma)</div>
<div class="option wrong">B. Th2 cells</div>
<div class="option wrong">C. Th17 cells</div>
<div class="option wrong">D. Treg cells</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p><strong>Th1 cells</strong> secrete <strong>IFN-γ</strong>, which activates macrophages to kill intracellular pathogens and form <strong>granulomas</strong> to wall off organisms that are hard to kill (e.g., <strong>Mycobacterium tuberculosis</strong>). This case is classic TB: returned from endemic area, productive cough, weight loss, hilar lymphadenopathy. Granuloma = epithelioid macrophages + giant cells + lymphocytes. Th1 also increases MHC class I and II expression.</p>
</div>
<div class="key-fact">🔑 Th1: IFN-γ → macrophage activation → granuloma | Targets: M.tb, Listeria, fungi (Histoplasma, Coccidioides)</div>
<span class="tag clinical">Clinical</span><span class="tag high">High Yield</span>
</div>
<!-- Q26 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">26</div>
<div class="q-text">A child develops asthma and elevated IgE levels with marked eosinophilia. Which Th subset and its cytokines are driving this response?</div>
</div>
<div class="options">
<div class="option wrong">A. Th1 (IFN-γ)</div>
<div class="option correct">B. Th2 (IL-4, IL-5, IL-13)</div>
<div class="option wrong">C. Th17 (IL-17, IL-22)</div>
<div class="option wrong">D. Treg (IL-10, TGF-β)</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p><strong>Th2 cells</strong> secrete <strong>IL-4</strong> (drives IgE production → allergy; also drives Th2 differentiation), <strong>IL-5</strong> (activates/increases eosinophils), and <strong>IL-13</strong> (increases mucus secretion). Th2 responses are necessary for defense against <strong>helminth parasites</strong> but pathogenic in <strong>allergic diseases</strong> (asthma, atopy). The <strong>IgE + eosinophil axis</strong> is the hallmark of Th2-driven pathology.</p>
</div>
<div class="key-fact">🔑 Th2: IL-4 (IgE↑) + IL-5 (eosinophils) + IL-13 (mucus) → allergy/asthma + anti-helminth</div>
<span class="tag clinical">Clinical</span><span class="tag high">High Yield</span>
</div>
<!-- Q27 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">27</div>
<div class="q-text">Which Th subset specifically recruits neutrophils to mucosal surfaces and helps maintain mucosal barrier integrity via IL-22?</div>
</div>
<div class="options">
<div class="option wrong">A. Th1</div>
<div class="option wrong">B. Th2</div>
<div class="option correct">C. Th17</div>
<div class="option wrong">D. Tfh</div>
<div class="option wrong">E. Treg</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p><strong>Th17 cells</strong> secrete <strong>IL-17</strong> (attracts neutrophils → phagocytosis of extracellular bacteria and fungi) and <strong>IL-22</strong> (stimulates epithelial cells to produce antimicrobial peptides; maintains mucosal barrier). Th17 cells are important in defense against <strong>extracellular bacteria and fungi</strong>. Defects in Th17 → susceptibility to <em>Candida</em> and <em>Staphylococcus aureus</em>.</p>
</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q28 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">28</div>
<div class="q-text">Regulatory T cells (Treg) suppress excessive immune responses. Which cytokines do they produce, and what cell marker identifies them?</div>
</div>
<div class="options">
<div class="option wrong">A. IFN-γ and TNF; CD8 marker</div>
<div class="option wrong">B. IL-17 and IL-22; CD17 marker</div>
<div class="option correct">C. IL-10 and TGF-β; CD25 marker (also FoxP3 transcription factor)</div>
<div class="option wrong">D. IL-4 and IL-5; CD4 marker only</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p><strong>Tregs</strong> express <strong>CD4, CD25 (high)</strong> and transcription factor <strong>FoxP3</strong>. They produce anti-inflammatory cytokines <strong>IL-10</strong> and <strong>TGF-β</strong> that suppress helper and cytotoxic T cell activity, preventing autoimmunity and excessive inflammation. They shut down immune responses after the pathogen is cleared. TGF-β also increases isotype switching to <strong>IgA</strong>.</p>
</div>
<div class="key-fact">🔑 Treg: CD4+CD25+FoxP3+ | IL-10 + TGF-β | Suppress autoimmunity; shut down immune response</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q29 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">29</div>
<div class="q-text">Cytotoxic T cells (CTLs) kill virus-infected cells by two mechanisms. Which statement is CORRECT?</div>
</div>
<div class="options">
<div class="option wrong">A. They release antibodies that coat the infected cell</div>
<div class="option wrong">B. They activate complement to lyse infected cells</div>
<div class="option correct">C. They release perforin (pores) + granzymes (apoptosis) and express FasL to trigger Fas-mediated apoptosis</div>
<div class="option wrong">D. They release IL-4 to attract eosinophils to kill the cell</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p>CTL (CD8+) killing mechanisms: ❶ <strong>Perforin</strong> creates pores in target cell membrane → <strong>Granzymes</strong> enter and activate caspases → <strong>apoptosis</strong>. ❷ CTL expresses <strong>FasL (Fas Ligand)</strong>, binds to <strong>Fas receptor</strong> on target cell → <strong>apoptosis signaling</strong>. Both mechanisms induce programmed cell death (apoptosis), not lysis. CTLs recognize antigen on <strong>MHC class I</strong> (CD8 restricted). They kill virus-infected cells, tumor cells, and transplanted tissue.</p>
</div>
<span class="tag high">High Yield</span>
</div>
<!-- Q30 -->
<div class="mcq-card">
<div class="q-header">
<div class="q-num">30</div>
<div class="q-text">ACTIVE vs PASSIVE immunity — which statement is CORRECT?</div>
</div>
<div class="options">
<div class="option wrong">A. Passive immunity has a long duration and slow onset</div>
<div class="option wrong">B. Active immunity provides immediate protection but no memory</div>
<div class="option correct">C. Passive immunity provides immediate protection (antibody only) but short duration (months); Active immunity has slow onset but long duration (years)</div>
<div class="option wrong">D. Both active and passive immunity involve T cell activation</div>
</div>
<div class="answer-box">
<div class="label">✏️ Explanation</div>
<p><strong>Active immunity</strong>: Host produces own antibodies + T cells (long duration, years; slow onset). Example: vaccination. <strong>Passive immunity</strong>: Preformed antibodies given (immediate protection; short duration, months — antibodies degrade). Examples: tetanus antitoxin, rabies immunoglobulin, maternal IgG via placenta, IgA via breast milk. Key: passive = <strong>antibody only</strong> (no T cells, no memory).</p>
</div>
<div class="key-fact">🔑 Active: slow onset, long duration, antibody + T cells | Passive: immediate, short duration, antibody only</div>
<span class="tag high">High Yield</span>
</div>
</div><!-- end section 4 -->
<!-- QUICK REFERENCE SUMMARY TABLE -->
<div style="max-width:900px; margin: 30px auto 10px; background:white; border-radius:12px; padding:25px 30px; box-shadow:0 2px 12px rgba(0,0,0,0.08);">
<h2 style="color:#1a237e; margin-bottom:15px; border-bottom:2px solid #e3e8f0; padding-bottom:8px;">⚡ Quick-Reference Cheat Sheet</h2>
<table style="width:100%; border-collapse:collapse; font-size:0.88em;">
<thead>
<tr style="background:#1a237e; color:white;">
<th style="padding:8px 12px; text-align:left;">Topic</th>
<th style="padding:8px 12px; text-align:left;">Must-Know Fact</th>
</tr>
</thead>
<tbody>
<tr style="background:#f5f5f5;"><td style="padding:7px 12px; font-weight:600;">PAMPs</td><td style="padding:7px 12px;">LPS, peptidoglycan, dsRNA — recognized by TLRs (PRRs)</td></tr>
<tr><td style="padding:7px 12px; font-weight:600;">Innate vs Adaptive</td><td style="padding:7px 12px;">Innate: fast, no memory, germline | Adaptive: slow, memory, somatic recombination</td></tr>
<tr style="background:#f5f5f5;"><td style="padding:7px 12px; font-weight:600;">CF</td><td style="padding:7px 12px;">Thick mucus → impaired mucociliary escalator → Pseudomonas infections</td></tr>
<tr><td style="padding:7px 12px; font-weight:600;">Defensins</td><td style="padding:7px 12px;">α = neutrophils + Paneth cells | β = epithelial cells | Pore-forming</td></tr>
<tr style="background:#f5f5f5;"><td style="padding:7px 12px; font-weight:600;">CRP</td><td style="padding:7px 12px;">Binds phosphorylcholine on bacteria → complement activation + opsonin | 1000× rise in infection</td></tr>
<tr><td style="padding:7px 12px; font-weight:600;">IL-8</td><td style="padding:7px 12px;">Main chemokine for granulocytes (neutrophils) | Key component of pus</td></tr>
<tr style="background:#f5f5f5;"><td style="padding:7px 12px; font-weight:600;">Complement pathways</td><td style="padding:7px 12px;">Classical (IgG/IgM) | Alternative (Factor B/D/Properdin, no Ab) | Lectin (MBL+MASP)</td></tr>
<tr><td style="padding:7px 12px; font-weight:600;">C3 convertases</td><td style="padding:7px 12px;">Classical: C4b2b | Alternative: C3bBb (stabilized by Properdin)</td></tr>
<tr style="background:#f5f5f5;"><td style="padding:7px 12px; font-weight:600;">C5a</td><td style="padding:7px 12px;">Most potent chemotactic factor | Anaphylatoxin | Neutrophil adhesion</td></tr>
<tr><td style="padding:7px 12px; font-weight:600;">MAC</td><td style="padding:7px 12px;">C5b-9 | Pore formation → lysis | Deficiency → Neisseria susceptibility</td></tr>
<tr style="background:#f5f5f5;"><td style="padding:7px 12px; font-weight:600;">HAE</td><td style="padding:7px 12px;">C1 INH deficiency → angioedema (no urticaria)</td></tr>
<tr><td style="padding:7px 12px; font-weight:600;">PNH</td><td style="padding:7px 12px;">DAF (CD55) + CD59 loss → RBC hemolysis (dark urine)</td></tr>
<tr style="background:#f5f5f5;"><td style="padding:7px 12px; font-weight:600;">IgG</td><td style="padding:7px 12px;">Crosses placenta | Opsonization | Complement | ADCC (NK) | Secondary response</td></tr>
<tr><td style="padding:7px 12px; font-weight:600;">IgA</td><td style="padding:7px 12px;">Secretions/breast milk | Mucosal immunity | Dimeric in secretions</td></tr>
<tr style="background:#f5f5f5;"><td style="padding:7px 12px; font-weight:600;">IgM</td><td style="padding:7px 12px;">Pentamer | First in primary response | Most efficient complement activation</td></tr>
<tr><td style="padding:7px 12px; font-weight:600;">IgE</td><td style="padding:7px 12px;">Allergy (mast cell/basophil) | ADCC against helminths (eosinophils)</td></tr>
<tr style="background:#f5f5f5;"><td style="padding:7px 12px; font-weight:600;">Papain</td><td style="padding:7px 12px;">2 Fab + 1 Fc | Pepsin: F(ab')₂</td></tr>
<tr><td style="padding:7px 12px; font-weight:600;">CD4 vs CD8</td><td style="padding:7px 12px;">CD4 + MHC II → helper | CD8 + MHC I → cytotoxic</td></tr>
<tr style="background:#f5f5f5;"><td style="padding:7px 12px; font-weight:600;">Th1</td><td style="padding:7px 12px;">IFN-γ | Macrophage activation | Granuloma | Intracellular pathogens (TB, Listeria, fungi)</td></tr>
<tr><td style="padding:7px 12px; font-weight:600;">Th2</td><td style="padding:7px 12px;">IL-4 (IgE↑) + IL-5 (eosinophils) + IL-13 (mucus) | Allergy/asthma, helminths</td></tr>
<tr style="background:#f5f5f5;"><td style="padding:7px 12px; font-weight:600;">Th17</td><td style="padding:7px 12px;">IL-17 (neutrophil recruitment) + IL-22 (mucosal barrier) | Extracellular bacteria/fungi</td></tr>
<tr><td style="padding:7px 12px; font-weight:600;">Treg</td><td style="padding:7px 12px;">CD4+CD25+FoxP3+ | IL-10 + TGF-β | Suppresses autoimmunity</td></tr>
<tr style="background:#f5f5f5;"><td style="padding:7px 12px; font-weight:600;">CTL killing</td><td style="padding:7px 12px;">Perforin + Granzymes → apoptosis | FasL-Fas → apoptosis</td></tr>
<tr><td style="padding:7px 12px; font-weight:600;">Active vs Passive</td><td style="padding:7px 12px;">Active: slow, long (years), Ab+T cells | Passive: immediate, short (months), Ab only</td></tr>
</tbody>
</table>
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<p>Batterjee Medical College · Microbiology Department · Immunology MCQs</p>
<p>Based on lectures: Levinson Review of Medical Microbiology & Roitt's Essential Immunology</p>
<p style="margin-top:5px; font-size:0.8em;">30 high-yield MCQs covering all 4 lectures | Answers & explanations included</p>
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