1. The Concept of Immunity
Immunity: Latin immunis, exempt
Susceptibility: Lack of resistance to a disease, also known as Vulnerability
Innate immunity: Inborn
Adaptive immunity: Acquired, resistance to a specific pathogen

2. An Overview of the Body’s Defenses
ANIMATION Host Defenses: The Big Picture
Figure 16.1

3. First Line of Defense: I. Skin & Mucous Membranes
Keratin, a protective protein
Mucous membranes
Hairs
Cilia
Tears, Saliva, Urine, Vaginal secretions
Lysozyme

4. Ciliary Escalator
Figure 24.7

5. II. Normal Microbiota
Normal microbiota compete with pathogens for nutrients
Keep pH unfavorable for disease microbes

6. Second Line of Defense I. Blood components
Red Blood Cells
Transport O2 and CO2
White Blood Cells:
Neutrophils
Phagocytosis
Basophiles
Histamine
Eosinophils
Kill with toxin

7. Macrophage
Phagocytosis
Dendritic cells
Natural killer cells
Destroy target cells by apoptosis
T cells
Cell-mediated immunity
B cells
Produce antibodies
Platelets
Blood clotting

8. Differential White Cell Count
Percentage of each type of white cell in a sample of 100 white blood cells
Early and late in infection: Neutrophil then Macrophage
Neutrophils
60–70%
Basophils
0.5–1%
Eosinophils
2–4%
Monocytes
3–8%
Lymphocytes
20–25%

9. II. Lymphatic System Tissue + Fluid
Figure 16.5a

10. III. Phagocytosis Neutrophils Macrophage Presents Ag
Secret cytokines (lymphokines + interleukins)
Figure 16.6

11. IV. Inflammation Releasing histamine
Vasodilation (histamine, kinins, prostaglandins, and leukotrienes)
Redness
Swelling
Pain
Heat
Tissue repair and wall-off

12. Fever Abnormally high body temperature Body’s defensive mechanism
Increase enzyme activity and cytokine activity
Increase blood flow
Some bacteria can not survive at higher temperature
Disadvantage:
Tachycardia
Acidosis
Dehydration
44–46°C fatal

13. V. Antimicrobial Substances
Complements
C3a + C5a cause inflammation
C5b + C6 + C7 + C8 + C9 cause cell lysis

14. V. Antimicrobial Substances
Interferons
a- and b- interferon: Virus infected cells to produce AVPs
g- interferon: Neutrophils and macrophages
Limitations:
Side effects
Short lived
Only prevents, not stop viral synthesis
No effect on a number of cancers
Ion-binding Proteins
AMPs: Natural antibiotics

15. Types of Adaptive Immunity
Naturally acquired active immunity
Resulting from infection
Naturally acquired passive immunity
Transplacental or via colostrum
Artificially acquired active immunity
Injection of Ag (vaccination)
Artificially acquired passive immunity
Injection of Ab

17. Dual Nature of Adaptive Immunity
Figure 17.8

18. Dual Nature of Adaptive Immunity
Humoral immunity:
B-cells
Ag-Ab
Cellular immunity
T-cells
Cytokines
ANIMATION Humoral Immunity: Overview

19. I. Antigens It has to be large Ag determinants = epitopes
Hapten and Carrier

20. Antigens
Figure 17.1

21. Haptens
Figure 17.2

22. II. Antibodies They are immunoglobulins (Ig)
The antigen-binding sites recognize epitope and determine valence
Constant Region / Variable Region
Heavy Chain / Light Chain

23. Antibodies
Figure 17.3a,b

24. IgG Antibodies Monomer Most common and abundant (80%) Fix complement
Cross placenta
Enhance phagocytosis; neutralize toxins and viruses; protects fetus and newborn
Half-life = 23 days

25. IgM Antibodies Pentamer Agglutination Fix complement
Agglutinates microbes; first Ab produced in response to infection
Half-life = 5 days

26. IgA Antibodies Dimer 10–15% of serum Abs In secretions
Mucosal protection
Half-life = 6 days

27. IgD Antibodies Monomer In blood, in lymph, and on B cells
On B cells, initiate immune response
Half-life = 3 days

28. IgE Antibodies Monomer Allergic reactions; lysis of parasitic worms
Half-life = 2 days

29. III. B Cells
Diversity
Self – non-self discrimination
Memory

31. 1st exposure to Ag
First Clones
2nd exposure to Ag

32. T-independent Activation of B Cells
Figure 17.6

33. T-dependent Activation of B Cells
Figure 17.4

34. Ag
Response Ig
Memory
T-dependent
Proteins
Strong
IgG
Yes
T-independent
Polymers
(Lipid or
Polysaccharides)
Weak
IgM No

35. Clonal Selection
ANIMATION Humoral Immunity: Clonal Selection and Expansion
Figure 17.5

36. Clonal deletion: eliminates harmful B cells

37. Immune Responses to an Antigen
Figure 17.16

38. Immune Responses to an Antigen

39. Monoclonal Ab Production

40. The Results of Ag-Ab Binding
Destroy
Made unavailable
Figure 17.7

41. IV. Cellular Immunity T cells mature in the thymus
Thymic selection eliminates many immature T cells
T cells respond to Ag by T-cell receptors (TCRs)
T cells require antigen-presenting cells (APCs)

42. T Helper Cells CD4+ or TH cells (When activated) Produce cytokines
Help in B cell and Tc cell activation

43. T Cytotoxic Cells CD8+ or TC cells
Target cells are self carrying endogenous antigens
Activated into cytotoxic T lymphocytes (CTLs)
CTL causes apoptosis

44. T Cytotoxic Cells
Figure 17.11

45. T Regulatory Cells Treg cells Suppress T cells against self
CD4 and CD25 on surface
Suppress T cells against self

46. Antigen-Presenting Cells
Digest antigen
Ag fragments on APC surface with MHC
B cells
Dendritic cells
Activated macrophages
ANIMATION Antigen Processing and Presentation: MHC

47. A Dendritic Cell
Figure 17.13

48. Activated Macrophages
Figure 17.14

49. Natural Killer (NK) Cells
Granular leukocytes destroy cells that don’t express MHC I
Kill virus-infected and tumor cells
Attack parasites

50. Cells Communicate via Cytokines
Representative Activity
Interleukin-1 (IL-1)
Stimulates TH cells in presence of antigens; attracts phagocytes
Interleukin-2 (IL-2)
Proliferation of antigen-stimulated CD4+ T helper cells, proliferation and differentiation of B cells; activation of CD8+ T cells and NK cells
Interleukin-12 (IL-12)
Inhibits humoral immunity; activates TH1 cellular immunity
Cytokine
Representative Activity
Lymphokines
Induce the migration of leukocytes
TNF-α
Promotes inflammation
Hematopoietic cytokines
Influence differentiation of blood stem cells
IFN- and IFN-
Response to viral infection; interfere with protein synthesis
IFN-
Stimulates macrophage activity

51. Immunological Disorders
Hypersensitivity
Type I: Immediate or anaphylactic
Type II: Cytotoxic
Type III: Complex
Type IV: Delayed or Cell-mediated
Autoimmune
Immunodeficiency
Primary: Genetic, developmental defects
Secondary: Due to infection, cancer, malnutrition / stress

52. Type I Hypersensitivity (Anaphylactic)
IgE
Histamine

53. Type II Cytotoxic
ABO blood types
Hemolytic disease of the newborn:

54. Hemolytic Disease of the Newborn

55. Type III: Immune Complex
Serum Sickness:
Arthus Reaction:

56. Type IV: Delayed (Cell-mediated)
Contact dermatitis: Poison ivy
Tuberculin skin test
Feature: Always localized

57. Type I Type II Type III Type IV IgE IgG, IgM T cells Therapy Steroids
Main Mediator
IgE
IgG, IgM
T cells
Therapy
Desensitization, antihistamines , steroids, epinephrine
Steroids

58. Autoimmune Disease
Rhumatoids
Examples

59. Transplantation Issues
Rejection
Tolerance
Immunosuppression

60. Immunodeficiency Disorders
Primary
Agammaglobulinemia: No Ig
DiGeorge syndrome: Thymus undeveloped, no T cell
Severe combined immunodeficiency (SCID): Defect in IL12 gene
Secondary
AIDS
Leukemia

61. Precipitation Tests
Precipitation
Immunodiffusion

62. Agglutination Tests
Agglutination
Hemagglutination

63. Complement Fixation
Ab/Ag complex competition

64. Immunological Tests (cont.)
Neutralization
Immuno-
fluorescence

65. ELISA Tests

66. Western Blots
Protein profiling