Non Specific Immune Defense

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  • 1. Immunology Non-specific defenses I External defenses
  • 2. Organization of the immune system External defenses Internal defenses Anatomical barriers Body secretions and excretions Normal commensal flora Cilia Innate immunity Adaptive immunity Humoral immunity Cell-mediated immunity Phagocytic cells Chemicals Complement Acute phase proteins Cytokines etc. The immune system
  • 3. Figure 2-2
  • 4. Figure 2-3 The threat of invasion by pathogens and our protection against it:
  • 5. Figure 2-4 part 1 of 2 Many barriers prevent pathogens from crossing epithelia and colonizing tissues.
  • 6. Figure 2-4 part 2 of 2 Many barriers prevent pathogens from crossing epithelia and colonizing tissues.
  • 7. Anatomical barriers Skin Mucous membranes Body secretions and excretions Mucus Tears, saliva, urine (wash action Lysozyme in tears/nose/saliva Lactoperoxidase in breast milk Acid pH in sweat, gastric juices, urine, Vaginal secretions Zn 2+ and spermine in semen Normal commensal flora Inhibitory substances Competition for nutrients Cilia Ciliary staircase in lungs Summary: external defenses
  • 8. Non-specific defenses Internal defenses Innate immunity
  • 9. Figure 2-1 The response to an initial infection occurs in three phases.
  • 10. Figure 1-3 The cellular elements of blood arise from pluripotent hematopoietic stem cells in the bone marrow.
  • 11. Figure 1-4 part 1 of 3
  • 12. Figure 1-4 part 2 of 3
  • 13. Figure 1-4 part 3 of 3
  • 14. Figure 1-5 Lymphocytes are mostly small and inactive cells. Left panel: light micrograph of a small lymphocyte surrounded by red blood cells. Note condensed chromatin of the nucleus, indicating little transcriptional activity, relative absence of cytoplasm, and small size. Right panel: transmission EM micrograph, also shows absence of rough endoplasmic reticulum, another sign of functional activity.
  • 15. These are large, granular lymphoid-like cells with important functions in innate immunity. They lack antigen-specific receptors but can recognize virus-infected cells.
  • 16. Neutrofiel, eosinofiel, monosiet, megakariosiet / Neutrophil, eosinophil, monocyte, megakaryocyte Kolonievormende eenheid- granulosiet, eosinofiel, monosiet, megakariosiet (KVE-GEMMe) / Colony forming unit -granulocyte, eosinophil, monocyte, megakaryocyte (CFU-GEMMe) Multi-kolonie-stimulerende faktor (Multi-KSF) en IL3 / Multi-colony stimulating factor (Multi-CSF) and IL3 Neutrofiel, monosiet / Neutrophil, monocyte Kolonievormende eenheid-granulosiet -monosiete (KVE-GM) / Colony forming unit - granulocyte -monocyte (CFU-GM) Granulosiet -monosiete-kolonie-stimulerende faktor (GM-KSF) / Granulocyte -monocyte-colony stimulating factor (GM-CSF) Neutrofiel / Neutrophil Kolonievormende eenheid-granulosiet (KVE-G) / Colony forming unit-granulocyte (CFU-G) Granulosiet-kolonie-stimulerende faktor (G-KSF) / Granulocyte-colony stimulating factor (G-CSF) Monosiet / Monocyte Kolonievormende eenheid-monosiet (KVE-M) / Colony forming unit- monocyte (CFU-M) Monosiete-kolonie-stimulerende faktor (M-KSF) / Monocyte-colony stimulating factor (M-CSF) GEREGULEERDE KOLONIE / REGULATED COLONY TEIKENSEL / TARGET CELL FAKTOR / FACTOR
  • 17. Figure 2-5 Macrophages are activated by pathogens and both engulf them and initiate inflammatory responses.
  • 18. Figure 2-6 Macrophages produce and release bactericidal agents on ingestion of microorganisms.
  • 19. Figure 2-7 The respiratory burst in macrophages and neutrophils is caused by a transient increase in oxygen consumption during the production of microbicidal oxygen metabolites.
  • 20. Chronic granulomatous disease
    • These patients have a genetic deficiency of NADPH oxidase, which means that their phagocytes do not produce toxic oxygen derivatives.
    • They are less able to kill phagocyte-ingested microorganisms.
    • They are unusually susceptible to bacterial and fungal infections.
  • 21. Figure 2-8 Infection stimulates macrophages to release cytokines and chemokines that initiate an inflammatory response.
  • 22. Figure 2-9 Monocytes circulating in the blood recognize blood vessel walls near the site of inflammation and leave the bloodstream to migrate into the tissue toward the site of inflammation.
  • 23. Figure 2-10 Pattern recognition in the innate immune system: comparison of the characteristics of recognition molecules in the innate and adaptive systems.
  • 24. Figure 2-11 Mannose-binding lectin recognizes bacterial surfaces by their particular spacing of carbohydrate residues.
  • 25. Figure 2-12 Each of the 10 known TLRs recognize one or more microbial molecular patterns, mostly by direct interaction with molecules on the pathogen surface. These patterns are not found in normal vertebrates. As there are only 10 TLR genes, they have limited specificity, unlike receptors from the adaptive immune system. TLRs recognize a broad range of pathogenic microorganisms.
  • 26. Figure 2-13 Salmonella typhi (typhoid fever) invades directly through the epithelia. The long flagella are recognized by TLRs on macrophages and DCs and provoke an innate response.
  • 27. Figure 2-14
  • 28. Figure 2-39
  • 29. Figure 2-15
  • 30. Figure 2-41 part 1 of 2 Chemokines attract inflammatory cells. For illustration only.
  • 31. Figure 2-41 part 2 of 2
  • 32. Figure 2-45 Tumor necrosis factor- α has important local protective effects but can have severely detrimental effects systemically.
  • 33. Figure 2-46 TNF- α , IL-1 and IL-6 have a wide spectrum of biological activities that help to coordinate the body’s responses to infection.
  • 34. Figure 2-47 part 1 of 2 The acute phase response produces molecules that bind pathogens but not host cells.
  • 35. Figure 2-47 part 2 of 2
  • 36. Figure 2-16 Bacterial LPS induces changes in Langerhans’ cells, stimulating them to migrate and initiate adaptive immunity to infection by activating CD4 T cells.
  • 37. Figure 2-17