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Vip immunity to infections

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Vip immunity to infections

  1. 1. <ul><li>Immunity to infections </li></ul><ul><li>Prof M.I.N. Matee </li></ul>
  2. 2. About this Chapter <ul><li>Anatomy & function of immune system, organs, & cells </li></ul><ul><li>How the body defends itself </li></ul><ul><li>Non-specific body defenses </li></ul><ul><li>Specific defenses that target one pathogen </li></ul><ul><li>Combined defenses against bacteria and viruses </li></ul><ul><li>Allergies and autoimmune problems </li></ul>
  3. 3. Immune System Functions: Overview of Defenses <ul><li>Scavenge dead, dying or abnormal (cancerous) body cells </li></ul><ul><li>Protect from pathogens & foreign molecules </li></ul><ul><ul><li>Parasites </li></ul></ul><ul><ul><li>Bacteria </li></ul></ul><ul><ul><li>Viruses </li></ul></ul>
  4. 4. Immune System Functions: Overview of Defenses Figure 24-1: Viruses
  5. 5. Body Defenses: Overview <ul><li>Physical barriers: skin & epithelial linings & cilia </li></ul><ul><li>Chemical: acids, mucous & lysozymes </li></ul><ul><li>Immune defenses – internal </li></ul><ul><ul><li>Innate, non-specific, immediate response (min/hrs) </li></ul></ul><ul><ul><li>Acquired – attack a specific pathogen (antigen) </li></ul></ul><ul><li>Steps in Immune defense </li></ul><ul><ul><li>Detect invader/foreign cells </li></ul></ul><ul><ul><li>Communicate alarm & recruit immune cells </li></ul></ul><ul><ul><li>Suppress or destroy invader </li></ul></ul>
  6. 11. PRO-INFLAMMATORY CYTOKINES
  7. 12. Components of the Immune System Bacteria Entering B Cells T Cells Macrophage
  8. 13. The Innate Immune System Bacteria Entering NK Cells Phagocytosis Chemotaxis Virus Infected Cell Lysis
  9. 14. Innate and Adaptive Immune Responses Lysis Antibodies Plasma Cell Memory B cells Helper B Helper T Memory T cell Cytotoxic T cell Suppressor T cell Bacteria Entering Phagocytosis Chemotaxis Opsonization Antigen Presentation Virus infected cell
  10. 15. Lymphatic System: Overview of Immune Defense Organs & Cells <ul><li>Bone marrow </li></ul><ul><li>Thymus </li></ul><ul><li>Lymph nodes </li></ul><ul><li>Spleen </li></ul><ul><li>Lymph vessels </li></ul><ul><li>Leukocytes: </li></ul><ul><ul><li>(white blood cells – WBCs) </li></ul></ul>
  11. 16. Lymphatic System: Overview of Immune Defense Organs & Cells Figure 24-2 ab: Anatomy of the immune system
  12. 17. Key Cells & Overview of their Function in Immune Defense <ul><li>Lymphocytes: helper, plasma, cytotoxic & natural killer (NK) </li></ul><ul><li>Basophils </li></ul><ul><li>Mast cells </li></ul><ul><li>Monocytes </li></ul><ul><li>Macrophages </li></ul><ul><li>Neutrophils </li></ul><ul><li>Eosinophils </li></ul>
  13. 18. Key Cells & Overview of their Function in Immune Defense Figure 24-4: Cells of the immune system
  14. 19. <ul><li>Physical & chemical barriers </li></ul><ul><li>Phagocytosis: macrophages, neutrophils, NK cells </li></ul><ul><li>Engulf and digest recognized &quot;foreign&quot; cells – molecules </li></ul><ul><li>Inflammatory response </li></ul>Innate Immunity: Phagocytosis & Inflammation
  15. 20. Innate Immunity: Phagocytosis & Inflammation Figure 24-6: Phagocytosis
  16. 21. <ul><li>Histamines: from mast cells  swelling, edema, b. v . dilation </li></ul><ul><li>Interleukins: fever,  b.v. gaps  WBC's & proteins  infection </li></ul><ul><li>Bradykinin: pain & swelling </li></ul><ul><li>Membrane attack complex proteins </li></ul>Inflammatory Response: Cytokines Signal Initiation
  17. 22. Inflammatory Response: Cytokines Signal Initiation Figure 24-8: Membrane attack complex
  18. 23. <ul><li>Activate T lymphocytes: direct attack </li></ul><ul><li>Activate B lymphocytes to become: </li></ul><ul><ul><li>Memory cells: 2 0 immune response to that antigen </li></ul></ul><ul><ul><li>Plasma cells: antibodies – attack that antigen </li></ul></ul>Acquired Immunity: Antigen-Specific Responses
  19. 24. Acquired Immunity: Antigen-Specific Responses Figure 24-13: Functions of antibodies
  20. 25. <ul><li>T cell receptors: cell activated to antigen </li></ul><ul><li>Major histocompatability complex (MHC) </li></ul><ul><li>Helper T cells: </li></ul><ul><ul><li>Cytotoxic T cells: perforins, granzymes, (apoptosis) & Fas </li></ul></ul>T Lymphocytes: Cell Mediated Immunity
  21. 26. T Lymphocytes: Cell Mediated Immunity Figure 24-16: T lymphocytes and NK cells
  22. 27. <ul><li>Make membrane attack complex  kill bacteria </li></ul><ul><ul><li>Inflammation: + recruit phagocytes, B & T lymphocytes </li></ul></ul><ul><ul><li>(Acquired response  antibodies, cytotoxic Ts … if needed) </li></ul></ul>Defenses against Bacteria: Complement P Activates:
  23. 28. Defenses against Bacteria: Complement P Activates Figure 24-17: Immune responses to bacteria
  24. 29. <ul><li>Circulating antibodies inactivate or target virus (opsins) </li></ul><ul><li>Macrophage  inflammation, interferon, cell activation </li></ul><ul><ul><li>Helper, cytotoxic T, NK & B cells  plasma c.  antibodies </li></ul></ul>Viral Defense: Summary of Innate & Acquired Responses
  25. 30. Viral Defense: Summary of Innate & Acquired Responses Figure 24-18: Immune responses to viruses
  26. 31. Summary <ul><li>Body defends itself with barriers, chemicals & immune responses </li></ul><ul><li>WBCs and relatives conduct direct cellular attack: phagocytosis, activated NK & cytotoxic T cells and produce attack proteins (i.e. antibodies, complement, & membrane attack complex) </li></ul>
  27. 32. Summary <ul><li>Cytokines, communicate cell activation, recruitment, swelling, pain, & fever in the inflammation response </li></ul><ul><li>Defense against bacteria is mostly innate while viral defense relies more on acquired immune responses </li></ul><ul><li>Autoimmune diseases are a failure of self-tolerance </li></ul>
  28. 33. Viruses   NNatural Immunity   Virus infection directly induce the production of IFN, which inhibit viral replication and the expression of MHC molecules NK cells lyse virally infected cells. IFN enhance the activity of NK. TThus NK is the primary natural immune response to viral infection.   Acquired Immunity Ab are important during early viral infection. Ab prevents entry to the host cells and opsonize viral particle for phagocytosis. CTL is important for established infection. Both CD4 and CD8 CTLs participate.
  29. 34. Immunity to Extracellular Bacteria   Live in tissue space and induce inflammation and tissue destruction   Release toxins:   Endotoxin: bacteria cell wall components Exotoxin: secreted by bacteria. Toxins induce cell activation and modulate activities of kinases and other enzymes. Immunity to extracellular bacteria is aimed to eliminate the bacteria and neutralizing toxins.   Natural Immunity:   Phagocytes  Complement via the alternative pathway: C3b opsonize bacteria, C9 lyse bacteria and other by-products promote inflammation. Toxins could lead to the production of cytokins. Uncontrolled cytokine production could result in septic shock. Example: LPS activate macrophages to produce TNF   Adoptive Immunity Humoral immunity is the principal protective mechanism   IgG opsonize bacteria by binding to FcR on phagocytes.   IgG and IgM neutralizing bacteria and prevent binding to cells   Activate the complement system. C3b promotes phocytosis activity.   CD4 T cells help antibody production and produce cytokines to help phagocytosis. Some Toxin can be superantigens.
  30. 35. Intracellular Bacteria   Natural Immunity   Can survive with in phagocytes due to the ability to interfere with lysosome movement. Natural immunity are quite ineffective. Difficult to eradicate and could cause chronic infections NK cells are the main force against intracellular infection.   Acquired Immunity   Mainly CMI. Type I CD4 cells activated by released antigens will produce IFNgamma which activate macrophages (RO) to effectively kill. CD4 cells also help CD8 cells to kill.  Activated macrophages during DTH cause tissue injury. Chronic antigen stimulation leading to granulomas, the histological hallmark. Granulomas limit spread but also cause tissue function impairment.
  31. 36. PParasites   Parasites often have many stages. Some of the stage are in intermediate hosts.   Natural Immunity   Not effective  Whenever enter tissue or blood, parasite could survive and replicate. Complements are ineffective. Phagocytes could be replication factory.   Acquires Immunity   Diverse response to various parasites IgE and eosonophil are important for helminth infections. Driven by IL-4 and IL5. Eosinophil granules are toxic to helminthes. Granuloma formation to contain parasites and eggs. Intracellular parasite stimulate CTL.

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