__Lecture 17 Hypersenisitivty type IV - final.pptx

Hypersensitivity reaction IV

1. Type IV hypersensitivity (Delayed) Saleh Bahaj Prof. of Medical Microbiology/Immunology Lecture 17

2. Objectives By the end of this lecture the students should be able to:- I) Def. of Type IV II) Pathogenic type III) Test your self II) Chemical type

3. Type IV hypersensitivity I) Definition

4. I) Definition of Type IV hypersensitivity It’s a delayed type that initiated by sensitized TH1 or CD8 cells leading to tissue damage

5. I) Definition of Type IV hypersensitivity Delayed (1-2 days)

6. I) Definition of Type IV hypersensitivity No antibodies Y

7. I) Definition of Type IV hypersensitivity Sensitization is is required

8. II) Types Type IV hypersensitivity

9. II) Examples Chemical substances (CD8 & TH1 cells) B) Pathogenic (CD8 & TH1 cells)

10. II) Types Type IV hypersensitivity A) Chemical substances

11. A) Chemical substances Haptens

12. A) Chemical substances Soap Hair dyes Poison ivy Poison oak Nickle Jewelry

13. A) Chemical substances Contact dermatitis TH1 cells Tc cells

14. II) Types Type IV hypersensitivity A) Chemical substances Role of CD8 cells (Sensitization)

15. 1) Ag presentation Skin protein Same Chemical ( Hapten ) Chemical combined with skin protein

16. 2) Migration into R. lymph nodes APC migrates into lymph nodes to meets the specific TC cells (Activation)

17. 3) Activation of Tc 1 st signal MHCI & TCR-CD8 2 nd signal B7 & CD28 CD40 & CD40L

18. 3) Proliferation of Tc cells Memory TC cells Effector cells (Sensitized Tc cells)

19. 3) Sensitized Tc cells to circulation Effector Tc cells enter circulation Travel to the site of infection Re-enter circulation Degradation

20. II) Types Type IV hypersensitivity Role of Tc cells 2 nd exposure (Effector phase) Chemical substances & Pathogen

21. Skin protein Same Chemical ( Hapten ) Chemical combined with skin protein 1) Ag Presentation (2 nd exposure) Our cells

22. 2) Killing by Tc cells Our cells Effector CD8 kills by 1 st signal

23. 2) Killing by Tc cells Hapten + Protein enter the cells and presented in associated with MHCI

24. Tissue damage

25. II) Types Type IV hypersensitivity Chemical substances & Pathogen Role of TH1 cells

26. TH1 cells 1) Sensitization phase 2) Effector phase

27. TH1 cells 1) Sensitization phase 2) Effector phase

28. II) Types Type IV hypersensitivity Role of TH1 cells Sensitization Chemical substances & Pathogen

29. 1) Ag Presentation Skin protein Chemical ( Hapten ) Chemical combined with skin protein APC Pathogen IL-12

30. 2) Migration into R. lymph nodes APC migrates into lymph nodes to meets the specific TH cells (Activation)

31. 3) Activation of TH cells IL-12 IL-2 1 st signal MHCI & TCR-CD4 2 nd signal B7 & CD28 CD40 & CD40L

32. 4) Proliferation of TH1 cells Memory TH1 cells Effector cells These T cell Sensitized to substance

33. 5) Sensitized TH1 cells to circulation Effector TH1 cells enter circulation Travel to the site of infection Re-enter circulation

34. II) Types Type IV hypersensitivity Role of TH1 cells 2 nd exposure (Effector phase) Chemical substances & Pathogen

35. Skin protein Same Chemical ( Hapten ) Chemical combined with skin protein Langerhans cells Dendritic cells 1) Ag Presentation (2 nd exposure)

36. Langerhans cells Dendritic cells 2) TH1 cells leave circulation IL-2, γ INF & TNF β Sensitized

37. 3) Activation of macrophages IL-2, γ INF & TNF β Attract lymphocytes Attract macrophages

38. 3) Activation of macrophage γ INF Macrophages Activation Oxygen free radicals Nitric oxide Tissue damage + Cytokines (Type IV)

39. 3) Activation of macrophage Tissue damage Granuloma (Tissue damage)

40. II) Types Type IV hypersensitivity Lab. diagnosis of contact dermatitis

41. Lab. Diagnosis Contact dermatitis Patch test Contact dermatitis 1-2 days

42. Lab. Diagnosis Contact dermatitis

43. Examples Type IV hypersensitivity II) Types

44. Tuberculin test Accumulation of macrophages & lymphocytes PPD

45. Graft rejection TH1 cells & CD8 cells Type IV

46. Insulin dependent diabetes mellitus Type IV

47. Exercise-2 Outcomes

48. Exercise-2 What are the outcomes of Sensitization & Effector phases in type IV hypersensitivity?

49. Answer of Exercise-2 1) Sensitization phase Outcomes (7-10 days) Expansion of TH1 cells or (Tc) Memory TH1 cells or (Tc) They circulate via blood & Lymph

50. Answer of Exercise-2 2) Effector phase Outcomes (1-2 days) A) IL-2, INF- γ , GM-CSF & TNF production B) Attract lymphocytes C) Attract monocytes D) Activate macrophage E) Tissue damage (free radical + Cytokines) Killing by Tc

51. Exercise-3 Predict Key players

52. Answer of Exercise-3 1 APC 2 TH1 /CD8 3 Sensitization & Effector phases are needed

53. Conclusion Antigen APC-MHC-II APC-MHC-I + TH1 cells Macrophage Activation + Tc cells Destruction Tissue damage

54. III) Test yourself

55. Q1 A delayed hypersensitivity reaction is characterized by: Monocyte2-3 days Monocyte2-3 days Edema without a cellular infiltrate An infiltrate composed of neutrophils An infiltrate composed of helper T cells and macrophages An infiltrate composed of eosinophils

56. Q2 Monocyte2-3 days A delayed hypersensitivity reaction is characterized by: Monocyte2-3 days The main cell is TH1 cells Antibodies have a role The response is delayed Cytotoxic T cells also play a role

57. Q3 Monocyte2-3 days Hypersensitivity to penicillin and hypersensitivity to poison oak are both Monocyte2-3 days Mediated by IgE antibody Mediated by IgG & IgM antibody Initiated by Th2 cells Initiated by hapten

58. Q4 Monocyte2-3 days On the first exposure to antigen, T helper cells Monocyte2-3 days Become activated and increase in number cause inflammation Attract more macrophages Cause skin lesions

59. Q5 Monocyte2-3 days When T helper cells are exposed for the second time to hapten -peptide on antigen presenting cells, they Monocyte2-3 days Lyse cells using perforin Release cytokines that attract macrophages Make antibodies Kill macrophages

60. Q6 Monocyte2-3 days The lepromin test is used to determine what type of leprosy. What type of reaction that occurs Monocyte2-3 days Type I Type II Type III Type IV

61. Q7 Monocyte2-3 days Contact dermatitis can be caused by the following Monocyte2-3 days Cosmetics Metals Poison ivy Resins

62. Q8 Monocyte2-3 days The Induration & erythema reaction has a nodule filled with Monocyte2-3 days Mast cells Lymphocytes & Macrophages Eosinophils Neutrophil

63. Q9 Monocyte2-3 days The allergic reaction to cosmetics, soap & metals is mediated by Monocyte2-3 days Cytotoxic T cells IgG & complement TH1 cells IgE

64. Q10 Monocyte2-3 days Skin lesions due to hypersensitivity-IV appear Monocyte2-3 days 24 hours after first exposure to antigen 24 hours after second exposure to antigen 48–72 hours after first exposure to antigen 3 weeks after second exposure to antigen

65. Thank you