Immune System Flashcards

Question

Q: An essential component of antigen processing is… A. Return of antigen-processing cell to bone marrow B. A time interval of 7 days between internalization of antigen and its appearance on the cell surface C. Binding of complement to antigen-processing cell D. Association of modified antigen with major histocompatibility complex

Answer 1

Correct Answer: D. Association of modified antigen with major histocompatibility complex (MHC) ⸻ What is Antigen Processing? Antigen processing is the breakdown of foreign proteins (antigens) inside an immune cell into smaller pieces (peptides). These peptides are then loaded onto MHC molecules and moved to the cell surface to be shown to T cells, so the immune system knows what to fight. ⸻ What is MHC (Major Histocompatibility Complex)? MHC = “Molecular display board” MHC molecules are cell-surface proteins that hold up antigen fragments so that T cells can “see” them. There are two main classes: * MHC Class I * Found on all nucleated cells * Presents antigens from inside the cell (like viruses) * Interacts with CD8+ cytotoxic T cells * Think: “If something’s wrong inside, MHC I will flag it.” * MHC Class II * Found only on professional antigen-presenting cells (APCs) like dendritic cells, macrophages, B cells * Presents antigens from outside the cell (like bacteria or toxins) * Interacts with CD4+ helper T cells * Think: “MHC II = I help you” (Helper T cells) ⸻ Answer Choice Breakdown: * A. Return of antigen-processing cell to bone marrow – Incorrect. APCs don’t return to the bone marrow. After capturing antigen, they go to the lymph nodes to find T cells. * B. A time interval of 7 days… – Incorrect. There’s no required 7-day delay. Processing and presentation typically happen in less than a day. * C. Binding of complement to antigen-processing cell – Incorrect. Complement helps with pathogen destruction, not antigen presentation. * D. Association of modified antigen with MHC – Correct. This is the central step in antigen processing — presenting the antigen on the cell surface via MHC so T cells can recognize it. ⸻ Key Term Definitions: * Antigen-presenting cell (APC): A cell that captures, processes, and presents antigens to T cells (e.g., dendritic cells). * Antigen processing: Breaking down proteins into pieces and preparing them for display on MHC molecules. * MHC (Major Histocompatibility Complex): Proteins that act like molecular trays to hold and show antigens to T cells. ⸻ Memory Trick: * “MHC = Molecular Handshake with T cells” * “Processing = Chop + Load on MHC” * MHC I = Infected (intracellular) → CD8+ T cells * MHC II = Invaders (extracellular) → CD4+ T cells

Answer 2

Correct Answer: B. Natural killer cells are derived from the monocyte ⸻ Answer Choice Breakdown: * A. Monocytes circulate in the blood for about a day – True. Monocytes are precursors to macrophages and dendritic cells. They circulate in the bloodstream for ~1 day, then migrate into tissues where they mature. * B. Natural killer (NK) cells are derived from the monocyte – False (Correct). NK cells come from the lymphoid lineage, not the myeloid lineage like monocytes. NK cells are more closely related to T and B cells, though they act like part of the innate immune system. Monocytes become macrophages or dendritic cells, not NK cells. * C. Perforin and granzyme are mediators of cell death by NK cells – True. NK cells kill infected or cancerous cells using: * Perforin: creates pores in the target cell membrane * Granzyme: enters the cell and triggers apoptosis (programmed cell death) * D. PMNs combat microorganisms by the release of ROS – True. PMNs (polymorphonuclear leukocytes, mainly neutrophils) kill microbes by: * Phagocytosis * Releasing reactive oxygen species (ROS) — powerful chemicals that damage pathogens ⸻ Key Term Definitions: * Monocyte: A circulating white blood cell that differentiates into macrophages or dendritic cells. * NK Cell (Natural Killer): Lymphoid-derived cell that kills virus-infected or cancerous cells without prior sensitization. * Perforin/Granzyme: Proteins used by NK cells and cytotoxic T cells to kill targets. * PMNs (Polymorphonuclear neutrophils): First responders in innate immunity; release ROS to destroy pathogens. * ROS (Reactive Oxygen Species): Toxic oxygen-containing molecules that kill bacteria and fungi. ⸻ Memory Trick: * “NK cells = Natural born killers = from Lymphoid” * “Monocytes = Macrophages & dendritic cells = from Myeloid” * “Perforin punches, Granzyme kills” * “PMNs = Pathogen Melters with Neutrophil power”

Answer 3

Correct Answer: C. Eosinophil ⸻ What is the Humoral Response? The humoral immune response is part of adaptive immunity. It involves B cells producing antibodies to neutralize pathogens in body fluids (“humors”) — like blood and lymph. Key players in this response include: * B cells (make antibodies) * Helper T cells (CD4+) (help activate B cells) * Antigen-presenting cells (like dendritic cells and macrophages that show the antigen to T cells) ⸻ Answer Choice Breakdown: * A. B cell – True, involved. B cells are the main players in humoral immunity. Once activated (by antigen and T cell help), they become plasma cells and produce antibodies. * B. T cell – True, involved. Specifically, helper T cells (CD4+) help activate B cells by releasing cytokines and providing costimulatory signals. * C. Eosinophil – False (Correct Answer). Eosinophils are granulocytes involved in the innate immune response, especially in defense against parasites and in allergic reactions. They release toxic granules, but do not play a role in antibody production or humoral immunity. * D. Antigen-presenting cell (APC) – True, involved. APCs (like dendritic cells or macrophages) are crucial for starting the immune response. They display antigen on MHC II to helper T cells, which then help activate B cells. ⸻ Key Term Definitions: * Humoral immunity: Antibody-mediated immunity that fights pathogens in fluids. * B cells: Make antibodies. * Helper T cells (CD4+): Activate B cells during adaptive immunity. * Eosinophils: Kill parasites and respond to allergens — not involved in antibody production. * APCs (Antigen-presenting cells): Present antigens to T cells to trigger a response. ⸻ Memory Trick: * “Humoral = Humor = Fluid = Antibodies” * “B cells = Build antibodies” * “T helper = Teach B cells” * “Eosinophils = Enemies of parasites, not part of humoral”

Answer 4

Correct Answer: B. Apoptosis ⸻ What is Cell-Mediated Cytotoxicity? This is the process by which cytotoxic T cells (CD8+) or natural killer (NK) cells directly kill infected, tumor, or damaged cells. They release toxic proteins (like perforin and granzymes) that trigger apoptosis — a controlled, programmed form of cell death. ⸻ Answer Choice Breakdown: * A. Necrosis – Incorrect. * Necrosis is uncontrolled cell death caused by trauma or infection. * It leads to inflammation and leakage of cellular contents. * Cytotoxic cells avoid necrosis to prevent tissue damage. * B. Apoptosis – Correct. * Programmed cell death — the “clean” way to kill a target cell. * Triggered by granzymes and Fas–FasL interactions * Keeps surrounding tissue safe * No inflammation, just removal of the damaged cell * C. Proliferation – Incorrect. * Means cell growth and division, which is the opposite of the goal in cytotoxicity. * T and NK cells kill targets, they don’t make them multiply. * D. Hyperplasia – Incorrect. * Refers to an increase in the number of cells, typically due to hormonal signals or chronic irritation. * Not related to immune destruction. ⸻ Key Term Definitions: * Apoptosis: A tidy, energy-dependent process where the cell shrinks and dies without triggering inflammation. * Perforin: Pokes holes in the cell membrane to let granzymes in. * Granzyme: Enters through perforin pores to activate apoptosis enzymes (caspases). * Fas/FasL: Another cell-death pathway used by cytotoxic T cells. ⸻ Memory Trick: * “CD8 = Cell Death through Apoptosis” * “Perforin punches → Granzyme goes in → Cell shuts down” * Think: “Cytotoxic = Clean Kill”

Answer 5

Correct Answer: C. The response can be enhanced by repeated antigen exposure ⸻ What is the Innate Immune Response? The innate immune system is your body’s first line of defense — a fast, non-specific response that reacts the same way every time, regardless of prior exposure. It includes barriers, cells, and soluble molecules that act quickly to stop infections before they spread. ⸻ Answer Choice Breakdown: * A. It is less specific than acquired immunity – True. Innate immunity uses pattern recognition receptors (like TLRs) that detect general danger signals, not specific antigens. It doesn’t “remember” past infections. * B. Complement is a soluble mediator – True. The complement system includes proteins in plasma that help destroy microbes, attract immune cells, and enhance phagocytosis. It’s a key part of innate defense. * C. The response can be enhanced by repeated antigen exposure – False (Correct). This describes adaptive immunity, not innate. Only B and T cells in the adaptive system “learn” and respond more strongly after repeat exposure. * D. Acute-phase proteins are involved – True. Acute-phase proteins like CRP and fibrinogen are made by the liver during infection or inflammation and help with opsonization, clotting, and limiting damage. ⸻ Key Term Definitions: * Innate immunity: Immediate, general response present from birth. * Acquired (adaptive) immunity: Slower, specific, memory-based immune response. * Complement: Group of plasma proteins that lyse pathogens and attract immune cells. * Acute-phase proteins: Proteins whose levels change rapidly in response to infection. ⸻ Memory Trick: * “Innate = Immediate but Imprecise” * “Adaptive = Accurate and Advanced after exposure” * Only adaptive gets stronger with practice!

Answer 6

Correct Answer: B. There is no interaction with the acquired immune response ⸻ What is the Complement System? The complement system is a group of over 30 proteins that act in a cascade to: * Kill pathogens directly (via MAC, membrane attack complex) * Promote inflammation * Help phagocytes clear invaders (via opsonization) Although it’s part of the innate immune system, it interacts with the adaptive immune response, especially via antibodies. ⸻ Answer Choice Breakdown: * A. It functions to destroy membranes of infectious agents and promote an inflammatory response – True. The complement cascade can form the MAC complex, which punches holes in pathogen membranes. Complement fragments like C3a and C5a also promote inflammation and attract immune cells. * B. There is no interaction with the acquired immune response – False (Correct). Complement does interact with adaptive immunity. * The classical pathway is triggered by antibodies (IgG or IgM) binding to antigens. * Complement can also enhance antibody responses and help B cells. * C. Three pathways have been identified – True. The complement system can be activated in three ways: 1. Classical (antibody-dependent) 2. Lectin (mannose-binding) 3. Alternative (pathogen surfaces) * D. Activation occurs when components sequentially act on others – True. Complement activation happens via a cascade, where one component cleaves and activates the next, like a row of dominoes. ⸻ Key Term Definitions: * Complement system: A protein cascade that enhances immune defense. * MAC (Membrane Attack Complex): A ring-shaped complex that drills into membranes to lyse pathogens. * Opsonization: Marking a pathogen for easier phagocytosis. * C3a/C5a: Complement fragments that increase inflammation and recruit immune cells. ⸻ Memory Trick: * “Complement = Completes the immune response” * “3 Paths to Kill: Classical, Lectin, Alternative” * “B cells and antibodies? Complement’s on it!”

Answer 7

Correct Answer: D. Inhibiting hyaluronidase of bacteria ⸻ What is the Fc Region of an Antibody? The Fc (Fragment crystallizable) region is the tail portion of an antibody that interacts with: * Immune cells (like macrophages, neutrophils, NK cells) * Complement proteins It does not bind antigen — that’s the job of the Fab (antigen-binding) region. The Fc region helps trigger immune responses like: * Opsonization * Complement activation * Antibody-dependent cell-mediated cytotoxicity (ADCC) ⸻ Answer Choice Breakdown: * A. Complement activation – True, mediated by Fc. The Fc region of IgG and IgM activates the classical complement pathway by binding C1q. * B. Binding to phagocytes – True, mediated by Fc. Fc regions bind to Fc receptors (FcRs) on phagocytes (e.g., macrophages, neutrophils) → promotes opsonization and phagocytosis. * C. Binding to leukocytes – True, mediated by Fc. Fc regions can bind to leukocytes (like NK cells, basophils) via Fc receptors, activating functions like degranulation or cell killing. * D. Inhibiting hyaluronidase of bacteria – False (Correct). Antibodies don’t inhibit bacterial enzymes directly like hyaluronidase. Instead, they neutralize toxins or block attachment, but not by the Fc region. Also, this is not a standard or well-recognized immune mechanism. ⸻ Key Term Definitions: * Fc region: Constant tail of antibody that interacts with immune system (not antigen). * Complement activation: Triggered by IgG/IgM Fc regions; leads to pathogen lysis. * Opsonization: Tagging pathogens for phagocytosis. * ADCC (Antibody-Dependent Cellular Cytotoxicity): Killing cells via NK cell interaction with Fc. ⸻ Memory Trick: * “Fc = ‘Flag and Call’ zone” * It flags invaders (for complement) * It calls immune cells (phagocytes, NK cells) * Fab = Finds Antigen, Fc = Calls for backup

Answer 8

Correct Answer: A. Basophils ⸻ What Are Antigen-Processing Cells (APCs)? Antigen-processing cells are immune cells that ingest antigens, process them, and present peptide fragments on MHC molecules to T cells. These include: * Dendritic cells (most potent APCs) * Macrophages * B cells (technically also APCs) ⸻ Answer Choice Breakdown: * A. Basophils – False (Correct). * Basophils are granulocytes involved in allergic reactions and parasite defense. * They release histamine and cytokines, but do not process or present antigens. * B. Macrophage – True. * Macrophages phagocytose pathogens, digest them, and present antigens on MHC II. * They are professional APCs. * C. Follicular dendritic cells – True. * Found in lymph node follicles, they trap antigen-antibody complexes and present them to B cells, helping in germinal center formation. * While they don’t process antigens the traditional way, they are involved in antigen display and humoral immunity support. * D. Langerhans dendritic cells – True. * These are skin-resident dendritic cells. * They capture and process antigens, then migrate to lymph nodes to activate T cells. ⸻ Key Term Definitions: * Antigen-presenting cell (APC): A cell that processes and displays antigens to T cells via MHC. * Basophils: Innate immune cells that release histamine, involved in allergy and parasite defense. * Dendritic cells: Best APCs for activating naïve T cells. * Langerhans cells: Specialized dendritic cells in the skin. ⸻ Memory Trick: * “Basophils Blast histamine, not antigens” * “Dendritic = Display duty” * “Macrophage = Munches and Presents” * FDC = Facilitates B cell memory in follicles

Answer 9

Correct Answer: C. Influenza ⸻ Concept Summary: People with mild to moderate immune suppression (e.g., from aging, chronic illness, steroids, or stress) are at greater risk for common respiratory viruses like influenza, which the immune system usually controls well in healthy individuals. More severe immune suppression opens the door to opportunistic infections by fungi and protozoa, which are rare in the general population. ⸻ Answer Breakdown with Illness Descriptions: * A. Protozoans – Usually severe suppression only. Protozoan infections include: * Toxoplasmosis (often from cats or undercooked meat) * Cryptosporidiosis (severe diarrhea from contaminated water) * Giardiasis (intestinal infection from water) These pathogens are usually handled well unless the person has very low T cell counts, as seen in AIDS or transplant recipients. * B. Candida albicans – Moderate to severe suppression. * A fungus that normally lives on skin and mucous membranes. * Can cause oral thrush, vaginal yeast infections, or systemic candidiasis in immunocompromised hosts. * Common in diabetics, cancer patients, or those on antibiotics/steroids. * C. Influenza – Correct answer. Common in mild suppression. * Respiratory virus that causes fever, cough, body aches. * Most people recover, but those with even mild immune deficits (like older adults, smokers, or stressed individuals) can have complications like pneumonia or hospitalization. * It’s a classic example of an early-warning illness for declining immunity. * D. Pneumocystis carinii (aka P. jirovecii) – Advanced suppression only. * Causes Pneumocystis pneumonia (PCP), an AIDS-defining illness. * Rare in healthy people, but common in HIV+ patients with CD4 < 200, transplant recipients, or those on prolonged steroids. * Presents with dry cough, hypoxia, fever, and “ground-glass” opacities on chest imaging. ⸻ Key Definitions: * Opportunistic infection: One that usually doesn’t cause disease unless the immune system is weakened. * Mild immune suppression: Can result from age, chronic stress, illness, or corticosteroids. * Severe immune suppression: Seen in AIDS, chemotherapy, bone marrow transplants, etc. ⸻ Memory Trick: * Mild = Mainstream bugs (Flu, colds) * Moderate = Mushrooms (Candida) * Severe = Sneaky protozoa & fungal invaders * “Flu Finds the Weak First” — flu hits early, other bugs wait for deeper suppression

Answer 10

Correct Answer: D. Prolonged human exposure can result in death from immunodeficiency ⸻ Context Overview: Halogenated aromatic hydrocarbons (HAHs), like TCDD (dioxin) and related compounds, are environmental contaminants known for their potent immunotoxicity in animal studies, especially in mice. They alter immune function largely through the Aryl Hydrocarbon Receptor (AHR). ⸻ Answer Choice Breakdown: * A. They are particularly immunotoxic in mice – True. Mice are highly sensitive to the immunotoxic effects of HAHs. Effects include thymic atrophy, reduced T-cell development, and weakened immune responses. * B. They are associated with thymic atrophy in animal models – True. One of the hallmark effects in animal studies is shrinking of the thymus, where T cells mature. This indicates impaired adaptive immunity. * C. Their effects are mediated through AHR – True. HAHs exert their biological effects by binding to the aryl hydrocarbon receptor (AHR), a transcription factor that regulates genes related to xenobiotic metabolism and immune function. * D. Prolonged human exposure can result in death from immunodeficiency – False (Correct). While HAHs alter immune function in humans, they have not been definitively shown to cause fatal immunodeficiency. * Human studies suggest subtle immunosuppression (e.g., altered cytokines, increased infection risk), but not direct mortality from immune failure as seen in animal studies. ⸻ Key Term Definitions: * HAHs (Halogenated Aromatic Hydrocarbons): Environmental toxicants like dioxins and PCBs. * AHR (Aryl Hydrocarbon Receptor): A ligand-activated transcription factor that mediates many toxicological effects of HAHs. * Thymic atrophy: Shrinkage of the thymus gland, often indicating T-cell developmental suppression. * Immunotoxicity: The harmful effects a chemical can have on the immune system. ⸻ Memory Trick: * “HAHs = Harm via AHR” * “Mice get the brunt, humans get the nudge” * Animal models show major effects (like thymic atrophy), but in humans, it’s more subtle and not fatal

Answer 11

Correct Answer: D. PBB – severe human immunodeficiency ⸻ Answer Breakdown: * A. Benzo[a]pyrene – metabolized by bone marrow – True pair. * Benzo[a]pyrene is a polycyclic aromatic hydrocarbon (PAH) that undergoes bioactivation in various tissues, including the bone marrow, where it can cause genotoxic effects. * Known for its role in chemical carcinogenesis and bone marrow suppression. * B. TCDD (2,3,7,8-Tetrachlorodibenzo-p-dioxin) – chloracne – True pair. * TCDD is a dioxin and a potent AHR ligand. * A classic symptom of dioxin exposure is chloracne, a severe acne-like skin condition. * C. PCDF (Polychlorinated dibenzofurans) – recurring respiratory infections – True pair. * PCDFs are environmental contaminants similar to dioxins. * Chronic exposure is associated with respiratory effects like infections, inflammation, and immune system alteration in animal studies. * D. PBB (Polybrominated biphenyls) – severe human immunodeficiency – False pair (Correct). * PBBs are flame retardants and structurally similar to PCBs, with potential for endocrine and immune disruption. * However, while they may cause mild immunotoxicity, they have not been definitively shown to cause severe immunodeficiency or death in humans. * This makes this pairing exaggerated and inaccurate. ⸻ Key Definitions: * Benzo[a]pyrene: Carcinogenic PAH, bioactivated in tissues, including marrow. * TCDD: A dioxin linked to immunotoxicity, chloracne, and thymic atrophy. * PCDFs: Related to dioxins; linked to respiratory and immune effects. * PBBs: Industrial chemicals; linked to mild immune and endocrine issues, not severe immunodeficiency. ⸻ Memory Trick: * “TCDD = Toxins Cause Dirty Dermis (chloracne)” * “Benzo = Burns bone marrow” * “PBB = Possibly Bad, but not deadly to immune system”

Answer 12

Correct Answer: B. The immunotoxicity of organophosphates is due to suppression of acetylcholinesterases ⸻ Why B is Incorrect: Organophosphates (OPs) do inhibit acetylcholinesterase (AChE) — that’s how they cause their acute neurotoxic effects. However, their immunotoxic effects are not primarily due to AChE inhibition. * Immunotoxicity is believed to be due to non-cholinergic mechanisms like: * Direct effects on immune cells * Disruption of cytokine signaling * Oxidative stress pathways ⸻ Answer Choice Breakdown: * A. Malathion demonstrates both immune suppression and immunoenhancement – True. * Malathion is an OP that has shown dual immunomodulatory effects depending on dose and exposure. * Can lead to decreased resistance to infection, or enhanced antibody production in certain conditions. * B. The immunotoxicity of organophosphates is due to suppression of acetylcholinesterases – False. * Correct in terms of neurotoxicity, but not for immunotoxicity, which involves alternative pathways. * C. Parathion suppresses both cell-mediated and humoral immunity – True. * Parathion exposure results in decreased T-cell function, antibody production, and lymphoid organ atrophy in animal models. * D. There is a correlation between DDE levels in breast milk and infant ear infections – True. * DDE (a breakdown product of DDT) has been linked to immune suppression in infants. * Studies show higher rates of otitis media (ear infections) with greater DDE exposure through breast milk. ⸻ Key Definitions: * Acetylcholinesterase (AChE): An enzyme that breaks down acetylcholine in the nervous system. * Organophosphates: Insecticides that inhibit AChE; examples include malathion and parathion. * Immunoenhancement: Abnormal stimulation of immune functions, which can lead to autoimmunity or hypersensitivity. * DDE (Dichlorodiphenyldichloroethylene): A persistent metabolite of the banned pesticide DDT. ⸻ Memory Trick: * “OPs zap nerves via AChE, but zap immunity through other means.” * “Malathion = Mixed effects” * “Parathion = Poor immune power” * “DDE = Dirty milk = ear infections”

Answer 13

Answer Choice Breakdown: * A. Zinc – Correct (Not immunosuppressive). * Zinc is essential for a well-functioning immune system. * It supports T cell development, wound healing, inflammation regulation, and antioxidant defense. * Zinc deficiency, not zinc itself, can impair immune function. * Supplementation can actually enhance immunity when deficient. * B. Arsenic – False (Is immunosuppressive). * Arsenic exposure suppresses T and B cell function, reduces cytokine production, and increases infection susceptibility. * Chronic exposure is associated with impaired vaccine response and autoimmunity. * C. Lead – False (Is immunosuppressive). * Lead disrupts both cell-mediated and humoral immunity, especially in children. * It alters T-helper cell function and suppresses antibody production. * Also affects the development of immune organs (e.g., thymus). * D. Mercury – False (Is immunosuppressive and immunostimulatory). * Mercury can suppress T-cell function but also stimulate autoantibody production, leading to autoimmunity. * Methylmercury in particular interferes with cytokine expression and macrophage activity. ⸻ Key Definitions: * Immunosuppressive agents: Chemicals or drugs that reduce the activity or effectiveness of the immune system. * Zinc: A micronutrient crucial for immune defense, antioxidant protection, and enzyme activity. * Heavy metals (As, Pb, Hg): Known toxicants that impair both innate and adaptive immunity. ⸻ Memory Trick: “Zinc = Zest for immunity. Heavy metals = Heavy harm.”

Answer 14

Correct Answer: D. All of the above ⸻ Answer Choice Breakdown: * A. Morphine increases CCR5 expression – True * CCR5 is a coreceptor that HIV uses to enter immune cells (like T cells). * Morphine can upregulate CCR5, making it easier for HIV to infect cells and spread. * B. Heroin use is associated with increased risk of HIV infection – True * Heroin users often engage in high-risk behaviors (e.g., needle sharing), directly increasing HIV exposure. * Heroin may also impair mucosal barriers and innate immunity, making infection more likely. * C. Opioid use may contribute to HIV progression through immune suppression – True * Opioids suppress both innate and adaptive immunity, reducing cytokine production and T-cell activity. * This can accelerate HIV progression and worsen clinical outcomes in infected individuals. * D. All of the above – Correct, as each individual statement is true. ⸻ Key Concepts: * CCR5: A chemokine receptor on T cells; major entry point for HIV. * Opioids and Immunity: Chronic opioid use weakens immune surveillance, promoting infection and viral replication. * HIV Progression: Suppressed immunity allows viral load to rise and CD4+ T cell count to fall. ⸻ Memory Trick: “Opioids Open the Door for HIV”: * Opioids * Overexpress CCR5 * Impair immunity * Drug use (like heroin) = High infection risk

Answer 15

Answer: A. Cocaine ⸻ Explanation: * Silica – A naturally occurring mineral found in sand, rock, and mineral ores. Inhalation of crystalline silica particles, especially in occupational settings (like mining or sandblasting), is a known trigger for autoimmune reactions, including scleroderma. * Vinyl chloride – A chemical used in making plastics (especially PVC). Chronic exposure has been linked to a scleroderma-like syndrome involving skin thickening and vascular symptoms. * Organic solvents – Liquids used to dissolve other substances, often found in paints, cleaners, and industrial processes. Long-term exposure has been linked in studies to autoimmune disorders, including systemic sclerosis. * Cocaine – A powerful stimulant drug that causes vasospasm (narrowing of blood vessels), which can mimic Raynaud’s phenomenon (a common symptom of scleroderma), but cocaine itself has not been causally linked to scleroderma in clinical studies. ⸻ Key Definitions: * Scleroderma (Systemic Sclerosis): A chronic autoimmune disease characterized by hardening and tightening of the skin and connective tissues, and may affect internal organs. * Raynaud’s phenomenon: A condition where small blood vessels in the fingers and toes constrict excessively in response to cold or stress, often turning them white or blue. Common in scleroderma. * Vasospasm: Sudden constriction of blood vessels, reducing blood flow. Can cause symptoms similar to Raynaud’s. * Autoimmune disease: A condition in which the immune system mistakenly attacks the body’s own tissues. ⸻ Memory Trick: S.V.O. – Silica, Vinyl chloride, and Organic solvents are the usual suspects in occupational exposure–related scleroderma. Cocaine just mimics symptoms but doesn’t cause it.

Answer 16

Answer: B. Carbon dioxide ⸻ Explanation: * Ozone (O₃) – A strong oxidant and air pollutant known to induce airway inflammation, increase bronchial hyperresponsiveness, and modify immune cell function in the lungs. * Sulfur dioxide (SO₂) – An irritant gas produced by fossil fuel combustion; it provokes bronchoconstriction and inflammation and can exacerbate allergic responses and asthma. * Nitrogen dioxide (NO₂) – A toxic component of vehicle exhaust and industrial emissions. It causes oxidative stress and modulates immune responses, contributing to respiratory disease and allergic sensitization. * Carbon dioxide (CO₂) – A naturally occurring gas involved in respiration and pH balance. It does not directly affect the immune function of the lung in the same way the above pollutants do. While elevated CO₂ levels can influence respiratory drive and acid-base status, it is not considered an immunotoxicant. ⸻ Key Definitions: * Pulmonary immunologic response: The immune system’s reaction within the lungs to harmful stimuli such as pathogens, allergens, or pollutants. * Bronchial hyperresponsiveness: Increased sensitivity of the airways to various stimuli, often seen in asthma. * Oxidative stress: Damage to cells caused by reactive oxygen species (free radicals), often triggered by air pollutants. * Irritant gas: A gas that causes inflammation and damage to mucous membranes upon inhalation. ⸻ Memory Trick: If it’s a common air pollutant, it probably affects the lungs’ immune defenses. CO₂ is more of a physiologic gas, not an environmental irritant.

Answer 17

Answer: C. Platinum ⸻ Explanation: * Chromium – A well-known skin sensitizer. Especially hexavalent chromium found in cement and leather products can cause allergic contact dermatitis. * Nickel – The most common metal allergen worldwide. Found in jewelry, coins, zippers, and eyeglass frames. A leading cause of contact dermatitis. * Cobalt – Often found alongside nickel in alloys and cosmetics. Can act as a co-sensitizer, contributing significantly to allergic reactions. * Platinum – While platinum salts (used in catalytic converters and industrial settings) are sensitizers and can cause respiratory allergies, metallic platinum itself is not typically associated with contact dermatitis. ⸻ Key Definitions: * Contact dermatitis: A skin reaction caused by direct contact with an allergen or irritant. Can be allergic (immune-mediated) or irritant (non-immune). * Sensitizer: A substance that can trigger an allergic immune response after repeated exposure. * Metal salts vs. metals: Metal salts (like platinum chloride) are often more reactive and more likely to cause immune responses than the pure elemental metal form. ⸻ Memory Trick: “Nickel, Cobalt, Chromium – the ‘Nick-Co-Cr’ dermatitis trio.” Platinum = “Pretty safe (as metal).” Just remember salts react, metals may not.

Answer 18

Answer: A. Pulmonary fibrosis ⸻ Explanation: * Asthma – Latex can cause occupational asthma through IgE-mediated allergic reactions or airway hyperresponsiveness after inhalation of latex particles, particularly in powdered gloves. * Urticaria – Latex contact can trigger immediate-type hypersensitivity reactions, including hives (urticaria), especially on areas of direct skin exposure. * Anaphylaxis – A severe, systemic, life-threatening Type I hypersensitivity reaction to latex proteins, especially in sensitized individuals (e.g., healthcare workers, patients with spina bifida). * Pulmonary fibrosis – This is not a recognized manifestation of latex allergy. Pulmonary fibrosis is a chronic interstitial lung disease involving progressive scarring, typically linked to occupational dusts, radiation, or certain medications—not allergens like latex. ⸻ Key Definitions: * Hypersensitivity: An exaggerated immune response to a substance that is normally harmless. * Latex allergy: An immune reaction to proteins found in natural rubber latex, often Type I (immediate, IgE-mediated) or Type IV (delayed, cell-mediated). * Urticaria: Also known as hives—raised, itchy welts on the skin resulting from an allergic reaction. * Anaphylaxis: A sudden, severe allergic reaction causing airway constriction, low blood pressure, and sometimes shock. * Pulmonary fibrosis: Scarring and thickening of lung tissue, leading to progressive respiratory difficulty; not allergic in origin. ⸻ Memory Trick: “Latex loves lungs, lips, and skin—but not scars.” → It can cause asthma (lungs), anaphylaxis (lips/throat), and urticaria (skin), but not fibrosis (scarring).

Answer 19

Answer: C. Commercial enzymes ⸻ Explanation: * Papain – A proteolytic enzyme derived from the papaya plant, widely used in meat tenderizers, pharmaceuticals, cosmetics, and some medical preparations. Known to be a potential allergen in occupational settings (especially among workers handling enzyme powders). * Subtilin – A bacterial enzyme (also called subtilisin), produced by Bacillus subtilis. It’s commonly used in detergents, cleaners, and industrial enzyme blends. Both are categorized as commercial enzymes and have been associated with occupational allergic reactions, such as asthma, rhinitis, and dermatitis. * Mold toxins – These are toxic metabolites (like aflatoxins) produced by fungi, not enzymes like papain or subtilin. * Mushroom toxins – Found in poisonous mushrooms (e.g., amanitin) and unrelated to commercial enzyme use. * Hypersensitivity agents in latex – These are specific latex proteins, not enzymes like papain or subtilin. ⸻ Key Definitions: * Commercial enzymes: Industrial enzymes used in various products (e.g., food processing, detergents, pharmaceuticals) to catalyze specific chemical reactions. * Proteolytic enzyme: An enzyme that breaks down proteins into peptides or amino acids. * Hypersensitivity: An exaggerated immune reaction to a substance, often involving IgE-mediated responses (Type I allergy). * Occupational asthma: A form of asthma triggered by inhaling fumes, gases, dust, or other potentially harmful substances at work. ⸻ Memory Trick: “Papain and subtilin = enzyme twins in industry.” Think: “P for Papain = Protein breaker in Products” and “S for Subtilin = Sudsy enzyme in Soaps.”

Answer 20

Answer: A. Risk assessment in immunotoxicology is a highly accurate exercise ⸻ Explanation: * A. Risk assessment in immunotoxicology is a highly accurate exercise – False. Immunotoxicology is a complex field where predicting health outcomes based on immune system changes is challenging. Immune responses vary widely between individuals and species, and subtle immune alterations may not always translate to clear clinical outcomes. Thus, risk assessment in this field is often limited in precision and considered a developing science. * B. Many chemicals can alter the immune system of animals – True. Numerous chemicals, such as heavy metals, pesticides, pharmaceuticals, and industrial pollutants, have been shown to cause immunosuppression, hypersensitivity, or autoimmune effects in animal models. * C. Perturbations in immune function can occur in the absence of any clinical observable effect – True. Immune biomarkers (like changes in cytokine levels or lymphocyte counts) can shift before symptoms appear, making early detection possible but interpretation difficult. * D. Alterations in immune function are correlated with an increased risk of infectious disease – True. Reduced immune competence (immunosuppression) can increase susceptibility to infections, particularly opportunistic pathogens. ⸻ Key Definitions: * Immunotoxicology: The study of the effects of chemicals or drugs on the immune system, including suppression, activation, or dysregulation. * Risk assessment: The process of evaluating the potential adverse health effects caused by chemical exposure. * Perturbation: A disturbance or alteration from normal function—here, of the immune system. * Biomarkers: Measurable indicators of biological states or conditions, such as cytokines or antibody levels. ⸻ Memory Trick: “Immunotoxicology is imperfectly predictive.” While chemicals can affect the immune system, we don’t yet fully predict who gets sick or how severely.

Answer 21

Answer: D. Contact hypersensitivity ⸻ Explanation: * The Buehler test is an in vivo assay used primarily in guinea pigs to assess a substance’s potential to cause delayed-type (Type IV) hypersensitivity, also known as contact hypersensitivity. * It’s considered one of the historical gold standard methods for skin sensitization, alongside the Guinea Pig Maximization Test (GPMT). * In the test, the animal is first sensitized to a substance and then challenged (re-exposed) on the skin. A hypersensitivity reaction (like redness or swelling) indicates sensitization. Incorrect options: * A. Autoimmunity – Refers to immune responses against self-antigens. This is not assessed with the Buehler test. * B. Pulmonary hypersensitivity – This involves respiratory sensitizers, usually assessed with inhalation or intranasal models, not dermal exposure. * C. Type III hypersensitivity reactions – Involve immune complex deposition, not skin sensitization; assessed with different models (e.g., Arthus reaction). ⸻ Key Definitions: * Contact hypersensitivity: A Type IV delayed hypersensitivity reaction typically occurring after skin contact with allergens (e.g., nickel, poison ivy). * Type IV hypersensitivity: Cell-mediated immune response involving T cells, not antibodies, with a delayed onset (24–72 hours after exposure). * Sensitization: The process of becoming allergic to a substance following repeated exposure. ⸻ Memory Trick: “Buehler = Body’s skin barrier response.” → Think: “Buehler tests the bump you get from skin contact allergens.”

Answer 22

Answer: A. Type I reaction ⸻ Explanation: * Type I hypersensitivity (also called immediate hypersensitivity) involves IgE antibodies and leads to rapid allergic reactions upon exposure to a sensitizing agent. In respiratory sensitization, inhaled allergens trigger mast cell degranulation, histamine release, bronchoconstriction, and airway inflammation — characteristic of asthma-like responses. * Common substances that cause respiratory sensitization include certain proteins, enzymes, isocyanates, and anhydrides. Animal models (especially rodents) are used to evaluate whether a substance induces this type of reaction. Incorrect options: * B. Type II reaction – Involves antibody-mediated cytotoxicity (e.g., hemolytic anemia); not related to airway sensitization. * C. Type III reaction – Involves immune complex deposition (e.g., serum sickness); not the mechanism for typical respiratory sensitization. * D. Autoimmune reaction – Targets self-antigens and involves dysregulation of immune tolerance, not sensitization by external allergens. ⸻ Key Definitions: * Respiratory sensitization: The development of allergic respiratory symptoms (like asthma or rhinitis) after inhalation exposure to a sensitizing agent. * Type I hypersensitivity: An IgE-mediated, immediate allergic response that can affect the skin, respiratory tract, or cause anaphylaxis. * IgE (Immunoglobulin E): An antibody involved in allergic responses; binds to allergens and triggers mast cell degranulation. * Mast cells: Immune cells that release histamine and other mediators in allergic reactions. ⸻ Memory Trick: “Type I takes your breath away” → Think respiratory issues = IgE-mediated, Immediate, Inflammatory = Type I

Answer 23

Answer: D. Adjuvant ⸻ Explanation: * Adjuvant – A substance that enhances the immune response to an antigen. In toxicology and immunology, adjuvants are used experimentally or in vaccines to boost immune activity. Some xenobiotics (foreign chemicals) can act as unintended adjuvants, leading to exaggerated immune responses. Other options: * A. Promoter – Usually refers to a compound that promotes tumor growth after initiation; not related to immune function enhancement. * B. Hapten – A small molecule that is not immunogenic on its own but can trigger an immune response when attached to a larger carrier protein. Haptens are more associated with allergic reactions, not immune enhancement. * C. Regulator – A general term and not a specific immunological classification for a substance that enhances immune function. ⸻ Key Definitions: * Xenobiotic: Any chemical substance foreign to the biological system (e.g., drugs, pollutants, synthetic chemicals). * Adjuvant: A compound that boosts or amplifies the body’s immune response to an antigen. * Antigen: A substance that is recognized by the immune system and can trigger an immune response. * Immune potentiation: The enhancement or upregulation of immune system activity, often by adjuvants. ⸻ Memory Trick: “Adjuvant = Add-to-jumpstart the immune system.” Think of “Adj-up the response!” when boosting immune activity.

Answer 24

Answer: C. Downregulation of the immune system

Answer 25

Explanation: Tertiary lymphoid tissues are structures that form in non-lymphoid organs during chronic inflammation, infection, or autoimmune conditions. They are not normally present but develop in response to immune stimuli. Examples include: * SALT (Skin-associated lymphoid tissue): involved in immune defense in the skin. * NALT (Nasal-associated lymphoid tissue): found in the upper respiratory tract. * Peyer’s patches: lymphoid nodules found in the small intestine (technically part of MALT but involved in mucosal immunity). The spleen, however, is a primary or secondary lymphoid organ, not tertiary. It is always present and involved in filtering blood and mounting immune responses to blood-borne pathogens. Memory tip: “Tertiary” = “temporary” structures formed after inflammation, not built-in organs like the spleen.

Answer 26

Explanation: T cells originate in the bone marrow but don’t mature there. Instead, they migrate to the thymus, where they learn to distinguish “self” from “non-self.” This is essential for developing immune tolerance and avoiding autoimmunity. Think “T” cells = Thymus to help remember. B cells, on the other hand, mature in the bone marrow (B = Bone marrow). Memory trick: “T cells take a trip to the Thymus.”

Answer 27

Correct Answer: C. Thymus Thymus: * Specialized organ where T cells mature. * Located in the upper chest, behind the sternum. * Most active during childhood. * “T” stands for thymus-derived. Memory trick: “T cells Train in the Thymus.” ⸻ Other Options: A. Spleen * Secondary lymphoid organ (not where T cells mature). * Filters blood and helps detect blood-borne pathogens. * Stores white blood cells (including mature T and B cells). * Think of it more as an immune “monitoring site,” not a training camp. B. Lymph nodes * Also secondary lymphoid tissue. * Filters lymph (fluid from tissues) and houses mature immune cells. * This is where T cells go to work, not where they mature. * Think: “Lymph nodes = immune battleground, not boot camp.” D. Peyer’s patches * Specialized lymphoid tissue in the small intestine. * Monitors gut pathogens and helps activate immune responses in the gut. * Not involved in T cell development.

Answer 28

A Explanation: * A. Collect antigens from the gastrointestinal tract True. Peyer’s patches are organized lymphoid follicles found in the small intestine, especially the ileum. They monitor gut bacteria and detect antigens, initiating immune responses. They’re part of GALT (gut-associated lymphoid tissue). * B. Are parts of the tonsillar tissue False. Tonsils are part of Waldeyer’s ring in the oropharynx, not the GI tract. Though both are mucosal lymphoid tissues, they’re in different regions. * C. Are located in the center of the spleen False. The spleen filters blood, not gut contents. Peyer’s patches don’t reside there. * D. Are located in the lung False. The lungs contain BALT (bronchus-associated lymphoid tissue), not Peyer’s patches. ⸻ Memory tip: “P” in Peyer’s = Patches in the Pepto-path (GI tract)

Immune System Flashcards

(52 cards)