Questions and Answers
Which component is cleaved by MASP-2 after MBL binds to a pathogen surface?
What role does C3b play in the complement system?
What phenotype is associated with a deficiency in C2 complement components?
Which complement deficiency is associated with lupus?
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Which outcome is indicated by host cells possessing inhibitors of complement?
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What role do tight junctions between epithelial cells play in innate immunity?
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Which component is most directly involved in the phagocytosis of pathogens?
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How does a low pH in the stomach contribute to innate immunity?
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Which pathway of complement activation would likely be compromised in someone with defective lymphocyte function?
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What is the primary function of antimicrobial factors secreted at epithelial surfaces?
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What is the primary mediator released by mast cells that causes vasodilation and increases vascular permeability during inflammation?
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Which of the following is NOT one of the basic stages of acute inflammation?
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Which hallmark of inflammation is associated with increased blood flow leading to redness?
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What is the effect of acute inflammation on lymph flow?
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According to historical medical observations, which of the following reflects the pain aspect of inflammation?
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What do PAMPs primarily indicate to the immune system?
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Which receptors are primarily responsible for recognizing DAMPs?
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What is the function of the inflammasome complex formed by some NLRs?
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What type of molecules can be classified as DAMPs?
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Toll-like receptors (TLRs) are primarily involved in recognizing which type of ligands?
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What is one key feature of epithelial surfaces that aids in innate immunity?
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What triggers the complement system in the innate immune response?
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Which cell types are primarily involved in the innate immune response?
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What is a characteristic of the acute inflammatory response?
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How does the innate immune system recognize 'non-self' entities?
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What distinguishes Pattern Recognition Receptors (PRRs) from other types of receptors in the immune system?
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Which of the following is a specific function of NOD-like receptors (NLRs)?
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Damage-Associated Molecular Patterns (DAMPs) primarily indicate what type of cellular state?
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How many Toll-like Receptors (TLRs) are known to exist in humans?
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Which of the following correctly defines PAMPs?
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What is a primary component that some active NLRs can induce?
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Which type of immune cell primarily expresses Pattern Recognition Receptors?
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Which of the following is NOT a common example of a DAMP?
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What key response is primarily triggered by the activation of Toll-like Receptors (TLRs)?
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What is one of the roles of extracellular heat-shock proteins in the context of DAMPs?
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Study Notes
Epithelial Barriers and Complement
- Epithelial surfaces serve as primary physical barriers in innate immunity, lined with cells that create tight junctions to prevent pathogen entry.
- Antimicrobial factors are secreted at epithelial surfaces, contributing to a hostile environment for pathogens.
- The complement system plays a crucial role in the innate immune response, activated through various pathways, including the lectin pathway mediated by Mannose-Binding Lectin (MBL).
- MBL binds pathogen surfaces, initiating a cascade that leads to the cleavage of complement proteins, ultimately tagging pathogens for destruction.
Cells of Innate Immunity & Inflammation
- Key innate immune cells include neutrophils and macrophages, which are essential for phagocytosis and the inflammatory response.
- Neutrophils have a short lifespan but are abundant in blood and respond rapidly to infection.
- Macrophages can reside in healthy tissues, have a longer lifespan, and initiate inflammation when damage occurs.
- Cytokines released by activated macrophages and other cells enhance immune responses and inflammation.
Inflammation Process
- Acute inflammation involves three stages: dilation of small blood vessels, increased permeability of microvasculature, and leukocyte extravasation.
- Symptoms of inflammation are characterized by Celsus’ hallmarks: redness (rubor), swelling (tumor), heat (calor), and pain (dolor).
- Inflammation is a protective response but can also lead to various pathologies if dysregulated.
Recognition of Non-Self and Damage
- The innate immune system recognizes non-self entities through Pattern Recognition Receptors (PRRs), which detect Pathogen-Associated Molecular Patterns (PAMPs) and Damage-Associated Molecular Patterns (DAMPs).
- PAMPs include microbial components like bacterial lipids and nucleic acids, whereas DAMPs consist of molecules released upon cell damage.
- TLRs (Toll-Like Receptors) and NLRs (NOD-Like Receptors) are types of PRRs crucial for sensing microbial and damage signals, activating proinflammatory pathways.
Complement System Outcomes and Deficiencies
- The complement system enhances pathogen targeting via opsonization (C3b tagging), promoting phagocytosis and lysis of pathogens.
- Complement deficiencies can lead to serious health issues: C1q deficiency is linked to lupus, C3 deficiency results in severe sepsis, and MAC deficiency predisposes to Neisseria infections.
Inflammation – Acute vs Chronic
- Acute inflammation typically results in edema and the recruitment of cells to combat pathogens, while chronic inflammation may lead to tissue damage and disease.
Learning Objectives Recap
- Distinguish between innate and adaptive immunity based on cell types and response kinetics.
- Explain the contributions of epithelial barriers and the complement system.
- Understand the importance of innate immune cells and the pathways leading to inflammation and tissue healing.
- Elucidate how the innate immune system recognizes threats through specific receptors and mechanisms.
Epithelial Barriers and Complement
- Epithelial surfaces include skin, lungs, gastrointestinal (GI) tract, and reproductive tract, providing crucial defense against pathogens.
- Epithelial tight junctions create a barrier that prevents pathogen entry, while mechanisms like mucociliary escalator and longitudinal flow contribute to mechanical protection.
- Chemical defenses include low pH in the stomach, fatty acids in the skin, and antimicrobial enzymes like lysozyme in tears and saliva.
- Healthy microbiomes in the skin, gut, and respiratory tract also play an essential role in innate immunity.
Cells of Innate Immunity & Inflammation
- Key innate immune cells:
- Macrophages: Tissue-resident, long-lived, derived from blood monocytes, initiate immune responses.
- Neutrophils: Short-lived, abundant, flood sites of inflammation to combat infection.
- Both macrophages and neutrophils utilize phagocytosis, employing receptors and opsonization via complement and antibodies to facilitate particle uptake.
Mechanisms of Phagocyte Action
- Phagocytosis involves the fusion of phagosomes with lysosomes, leading to degradation of pathogens.
- Reactive oxygen species are produced by key enzymes, NADPH oxidase and myeloperoxidase, essential for pathogen killing.
- Deficiencies in these enzymes can result in Chronic Granulomatous Disease, characterized by recurrent infections.
Complement System
- Complement components participate in innate immune response to combat infection, triggered by various pathways.
- Cleavage of C3 into C3a and C3b leads to:
- Phagocytosis of pathogens via opsonization.
- Lysis of pathogens through the formation of the membrane attack complex.
- Activation of inflammatory responses, recruiting additional immune cells.
Recognition of Non-Self and Damage
- Pattern Recognition Receptors (PRRs) are essential for recognizing pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs).
- PAMPs: Conserved microbial structures, such as bacterial membranes and viral nucleic acids, recognized for signaling an immune response.
- DAMPs: Indicators of cellular damage, including extracellular heat-shock proteins and mitochondrial DNA.
Pattern Recognition Receptors
- Toll-Like Receptors (TLRs): Recognize extracellular microbial ligands; there are 10 TLRs in humans, inducing proinflammatory responses.
- NOD-like Receptors (NLRs): Cytosolic receptors activated by PAMPs and DAMPs, with 22 family members linked to the inflammasome complex and IL-1β release.
- PRRs are expressed by innate immune cells, activating them to initiate immune responses.
Inflammatory Response
- Acute inflammatory responses are characterized by key chemical mediators and cellular activities, aiding in pathogen clearance and healing.
- Key mediators include various interleukins (IL-1, IL-2, IL-3), which contribute to the signaling processes in inflammation.
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Description
Test your knowledge on innate immunity, including epithelial barriers, complement systems, and the cells involved in innate immune responses. This quiz covers essential elements like innate recognition of non-self and damage, vital for understanding the immune system's first line of defense.
