Innate Immunity & Complement - Dr. Hussein (PDF)
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LECOM School of Pharmacy
Dr. Hussein
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These are lecture notes on innate immunity and complement from Dr. Hussein. They contain definitions and key concepts regarding the topic, including components of innate immunity, physical and chemical barriers, cytokines, and the role of the complement system.
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INNATE IMMUNITY & COMPLEMENT – DR. HUSSEIN (3RD PPT) 1. What are the components of innate immunity? A: Physical barriers, phagocytes (neutrophils, monocytes, macrophages), NK cells, complement system, cytokines, and other plasma proteins. 2. What are the primary physical and chemical barriers of...
INNATE IMMUNITY & COMPLEMENT – DR. HUSSEIN (3RD PPT) 1. What are the components of innate immunity? A: Physical barriers, phagocytes (neutrophils, monocytes, macrophages), NK cells, complement system, cytokines, and other plasma proteins. 2. What are the primary physical and chemical barriers of innate immunity? A: Skin, stomach acidity, mucus, cilia, microflora, lysozyme in tears, and flushing of the urinary tract. 3. What are cytokines and their role in innate immunity? A: Cytokines are small soluble proteins produced by cells like macrophages, which mediate immune and inflammatory reactions, and act as communication tools among leukocytes. 4. Name two cytokines produced by macrophages. A: Tumor necrosis factor (TNF) and Interleukin-1 (IL-1). 5. Which type of cells are responsible for killing host cells infected by intracellular microbes? A: Natural killer (NK) cells. 6. What is the role of the complement system in innate immunity? A: The complement system aids in inflammation control, phagocytosis, and the lysis of bacteria and virus-infected cells. 7. Which cells produce Type I interferons (IFN-α and IFN-β)? A: IFN-α is produced by macrophages, and IFN-β is produced by fibroblasts. 8. What are toll-like receptors (TLRs), and what is their function? A: TLRs are pattern recognition receptors that recognize different components of bacterial cells and activate macrophages. 9. What are the main functions of activated macrophages? A: Phagocytosis of microbes, production of reactive nitrogen species, secretion of cytokines, and presenting antigens to T-cells. 10. How do NK cells stimulate macrophages? A: NK cells secrete IFN-γ, which activates macrophages to kill phagocytosed microbes. 11. What is the role of normal flora in immunity? A: Normal flora competes with pathogens on skin and mucosal surfaces, providing a protective effect. 12. Name two soluble factors involved in innate immunity. A: Lysozyme and complement proteins. 13. What are the toxic oxygen species produced by phagocytes during microbial killing? A: Oxygen radicals, hydrogen peroxide (H2O2), and hypochlorous acid (HOCl). 14. Define pathogen-associated molecular patterns (PAMPs). A: PAMPs are essential molecular structures, like polysaccharides, that are present on pathogens but absent in host cells. 15. What are pattern recognition receptors (PRRs)? A: PRRs are receptors in innate immunity that recognize PAMPs on microbes. 16. What differentiates innate immunity from adaptive immunity? A: Innate immunity has a broad, non-specific response, while adaptive immunity is highly specific and has memory of prior exposure. 17. What is C-reactive protein (CRP), and what is its function in immunity? A: CRP is a protein made in the liver that binds phosphocholine on microbes and activates the classical complement pathway. 18. How is CRP involved in inflammation? A: CRP neutralizes pro-inflammatory platelet-activating factor (PAF) and enhances phagocytosis of microbes. 19. What are defensins, and where are they found? A: Defensins are cationic proteins with antimicrobial activity, found in neutrophil granules and some macrophages. 20. What role do defensins play in protecting epithelial surfaces? A: They protect epithelial surfaces like skin and mucosal linings by killing bacteria, fungi, and viruses. 21. What is acute inflammation, and how is it initiated? A: Acute inflammation is an immediate response to infection or tissue damage, initiated by cytokine release from macrophages, dendritic cells, and mast cells. 22. What is the function of leukocyte extravasation during inflammation? A: It allows white blood cells to move from the bloodstream to the site of infection, where they destroy microbes and clear damaged cells. 23. What are the three pathways of complement activation? A: Classical pathway, alternative pathway, and lectin pathway. 24. What are the main roles of complement in body defense? A: Opsonization, inflammation promotion, and membrane attack complex (MAC)-mediated cell lysis. 25. What triggers the classical pathway of complement activation? A: Antigen-antibody complexes involving IgG or IgM. 26. Which pathway of complement activation does not require antibodies? A: The alternative pathway and the lectin pathway. 27. What are the key activators of the alternative complement pathway? A: Lipopolysaccharides (LPS), bacterial cell walls, and cobra venom. 28. What is the membrane attack complex (MAC)? A: A structure formed by complement proteins that creates pores in the membrane of pathogens, leading to cell lysis. 29. What are the split products of complement activation, and what are their roles? A: C3a and C5a; they function as anaphylatoxins promoting inflammation and chemotaxis. 30. What are the three functions of complement in host defense? A: Opsonization (C3b), chemotaxis (C5a), and cell lysis via MAC. 31. What is the significance of C3 in the complement system? A: C3 plays a central role in opsonization, immune complex clearance, and formation of the MAC. 32. How does complement contribute to bacterial clearance? A: By binding C3b to bacteria, enhancing phagocytosis, and promoting bacterial lysis. 33. What is the role of Factor D and Properdin in the alternative complement pathway? A: Factor D cleaves Factor B, and Properdin stabilizes the C3 convertase complex. 34. What is the role of C1 inhibitor in regulating complement activity? A: C1 inhibitor prevents uncontrolled activation of the classical complement pathway by inhibiting C1. 35. What is the cause of hereditary angioedema (HAE)? A: Deficiency of C1 inhibitor, leading to unregulated complement activity and edema. 36. How does the lectin pathway differ from the classical pathway of complement activation? A: The lectin pathway is activated by mannose-binding lectin binding to microbial surfaces, while the classical pathway requires antibody-antigen complexes. 37. What is the role of mannose-binding lectin (MBL) in complement activation? A: MBL binds to sugars on the surface of microbes, initiating the lectin pathway of complement activation. 38. What are some diseases associated with complement deficiencies? A: Increased susceptibility to infections like Haemophilus influenzae (alternative pathway defects) and Neisseria infections (C5 deficiency). 39. How can bacteria evade the innate immune system? A: Through mechanisms like capsule production, protease secretion, and inhibition of complement activation. 40. What is the importance of complement in linking innate and adaptive immunity? A: Complement activation helps stimulate adaptive immune responses by enhancing antigen presentation and promoting immune cell recruitment.