1. The Concept of Immunity
Susceptibility: Lack of resistance to a disease
Immunity: Ability to ward off disease
Innate immunity: Defenses against any pathogen
Adaptive immunity: Immunity, resistance to a specific pathogen

2. An Overview of the Body’s Defenses

3. The Concept of Immunity
Host Toll-like receptors (TLRs) attach to
Pathogen-associated molecular patterns (PAMPs)
TLRs induce cytokines that regulate the intensity and duration of immune responses

4. Physical Factors Skin Epidermis consists of tightly packed cells with
Keratin, a protective protein
Figure 16.2

5. Physical Factors Mucous membranes Mucus: Traps microbes
Ciliary escalator: Microbes trapped in mucus are transported away from the lungs

6. Normal Microbiota and Innate Immunity
Microbial antagonism/competitive exclusion: Normal microbiota compete with pathogens or alter the environment
Commensal microbiota: One organism (microbe) benefits and the other (host) is unharmed
May be opportunistic pathogens

7. Formed Elements in Blood
Red Blood Cells
Transport O2 and CO2
White Blood Cells:
Neutrophils
Phagocytosis
Basophiles
Histamine
Eosinophils
Kill parasites

8. Formed Elements in Blood
Monocytes
Phagocytosis
Dendritic cells
Natural killer cells
Destroy target cells

9. Formed Elements in Blood
T cells
Cell-mediated immunity
B cells
Produce antibodies
Platelets
Blood clotting

10. Differential White Cell Count
Percentage of each type of white cell in a sample of 100 white blood cells
Neutrophils
60–70%
Basophils
0.5–1%
Eosinophils
2–4%
Monocytes
3–8%
Lymphocytes
20–25%

11. Components of Lymphatic System
Figure 16.5a

12. Phagocytosis Phago: From Greek, meaning eat
Cyte: From Greek, meaning cell
Ingestion of microbes or particles by a cell, performed by phagocytes
Figure 16.6

13. Phagocytosis
Neutrophils
Fixed macrophages
Wandering macrophages

14. Phagocytosis
Figure 16.7

15. Microbial Evasion of Phagocytosis
Inhibit adherence: M protein, capsules
Streptococcus pyogenes, S. pneumoniae
Kill phagocytes: Leukocidins
Staphylococcus aureus
Lyse phagocytes: Membrane attack complex
Listeria monocytogenes
Escape phagosome
Shigella, Rickettsia
Prevent phagosome-lysosome fusion
HIV, Mycobacterium tuberculosis
Survive in phagolysosome
Coxiella burnettii

16. Inflammation
Acute-phase proteins activated (complement, cytokine, and kinins)
Vasodilation (histamine, kinins, prostaglandins, and leukotrienes)
Redness
Swelling (edema)
Pain
Heat

17. Chemicals Released by Damaged Cells
Histamine
Vasodilation, increased permeability of blood vessels
Kinins
Prostaglandins
Intensity histamine and kinin effect
Leukotrienes
Increased permeability of blood vessels, phagocytic attachment

18. The Process of Inflammation
Figure 16.8a, b

19. Phagocyte Migration and Phagocytosis
[Insert Animation Inflammation: Overview, Steps.]

20. Tissue Repair
Figure 16.8d

21. Fever Abnormally high body temperature
Hypothalamus normally set at 37°C
Gram-negative endotoxin cause phagocytes to release interleukin–1 (IL–1)
Hypothalamus releases prostaglandins that reset the hypothalamus to a high temperature
Body increases rate of metabolism and shivering which raise temperature
Vasodilation and sweating: Body temperature falls (crisis)

22. Fever Advantages Disadvantages Increases transferrins Tachycardia
Increases IL–1 activity
Produces Interferon
Disadvantages
Tachycardia
Acidosis
Dehydration
44–46°C fatal

23. The Complement System Serum proteins activated in a cascade
Activated by
Antigen-antibody reaction
Proteins C3, B, D, P and a pathogen

24. The Complement System C3b causes opsonization
C3a + C5a cause inflammation
C5b + C6 + C7 + C8 + C9 cause cell lysis

25. The Complement System
Figure 16.9

26. Effects of Complement Activation
Opsonization or immune adherence: Enhanced phagocytosis
Membrane attack complex: Cytolysis
Attract phagocytes
Figure 16.10

27. Some Bacteria Evade Complement
Capsules prevent C activation
Surface lipid-carbohydrates prevent membrane attack complex (MAC) formation
Enzymatic digestion of C5a

28. Interferons (IFNs)
IFN- and IFN-: Cause cells to produce antiviral proteins that inhibit viral replication
Gamma IFN: Causes neutrophils and macrophages to phagocytize bacteria

29. Antiviral Actions of Interferons (IFNs)
Figure 16.15

30. Innate Immunity Transferrins Antimicrobial peptides Bind serum iron
Lyse bacterial cells

31. Immunity Innate immunity: Defenses against any pathogen
Adaptive immunity: Induced resistance to a specific pathogen

32. Dual Nature of Adaptive Immunity
Figure 17.8

33. Dual Nature of Adaptive Immunity
T and B cells develop from stem cells in red bone marrow
Humoral immunity
B cells mature in the bone marrow
Chickens: Bursa of Fabricius
Due to antibodies

34. Dual Nature of Adaptive Immunity
T and B cells develop from stem cells in red bone marrow
Cellular immunity
Due to T cells
T cells mature in the thymus

35. The Nature of Antigens
Antigen (Ag): A substance that causes the body to produce specific antibodies or sensitized T cells
Antibodies (Ab) interact with epitopes or antigenic determinants
Hapten: Antigen is combined with carrier molecules

36. Antigens
Figure 17.1

37. The Nature of Antibodies
Globular proteins called immunoglobulins
The number of antigen-binding sites determines valence

38. IgG Antibodies Monomer 80% of serum Abs Fix complement
In blood, lymph, and intestine
Cross placenta
Enhance phagocytosis; neutralize toxins and viruses; protects fetus and newborn
Half-life = 23 days

39. IgM Antibodies Pentamer 5–10% of serum Abs Fix complement
In blood, in lymph, and on B cells
Agglutinates microbes; first Ab produced in response to infection
Half-life = 5 days

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

41. IgD Antibodies Monomer 0.2% of serum Abs
In blood, in lymph, and on B cells
On B cells, initiate immune response
Half-life = 3 days

42. IgE Antibodies Monomer 0.002% of serum Abs
On mast cells, on basophils, and in blood
Allergic reactions; lysis of parasitic worms
Half-life = 2 days

43. Activation of B Cells
Major histocompatibility complex (MHC) expressed on mammalian cells
T-dependent antigens
Ag presented with (self) MHC to TH cell
TH cell produces cytokines that activate the B cell
T-independent antigens
Stimulate the B cell to make Abs

44. Activation of B Cells
Figure 17.4

45. Clonal Selection
Figure 17.5

46. Activation of B Cells B cells differentiate into
Antibody-producing plasma cells
Memory cells
Clonal deletion eliminates harmful B cells

47. The Results of Ag-Ab Binding
Figure 17.7

48. T Cells and 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)
Pathogens entering the gastrointestinal or respiratory tracts pass through
M (microfold) cells over
Peyer’s patches, which contain APCs

49. T Helper Cells CD4+ or TH cells TCRs recognize Ags and MHC II on APC
TLRs are a costimulatory signal on APC and TH
TH cells produce cytokines and differentiate into
TH1
TH2
Memory cells

50. T Helper Cells
TH1 produces IFN-gwhich activates cells related to cell-mediated immunity, macrophages, and Abs
TH2 activate eosinophils and B cells to produce IgE

51. Activation of CD4+ T Helper Cells
Figure 17.10

52. T Cytotoxic Cells CD8+ or TC cells
Target cells are self carrying endogenous antigens
Activated into cytotoxic T lymphocytes (CTLs)
CTLs recognize Ag + MHC I
Induce apoptosis in target cell
CTL releases perforin and granzymes

53. T Cytotoxic Cells
Figure 17.11

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

55. Antigen-Presenting Cells
Digest antigen
Ag fragments on APC surface with MHC
B cells
Dendritic cells
Activated macrophages

56. Immunological Memory Antibody titer is the amount of Ab in serum
Primary response occurs after initial contact with Ag
Secondary (memory or anamnestic) response occurs after second exposure

57. Immune Responses to an Antigen
Figure 17.16

58. 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