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Flashcards in Unit 10 Deck (79):
1

Nonspecific (Innate) Defense System

-FIRST line of defense- skin & mucous membranes prevent microbe entry
-SECOND line of defense- antimicrobial proteins, phagocytic cells, etc.
-Inhibit spread of ALL invaders
-Rapid response time

2

Innate Defense (Surface Barriers)

-Skin & Mucous Membrane

3

Innate Defense (Internal Defenses)

-Phagocytes
-Fever
-NK Cells
-Antimicrobial Proteins
-Inflammation

4

Surface Barriers

Keratin (skin) & mucous membranes
-Physical Barrier
-Resistant to: acids & bases, bacterial enzymes & bacterial toxins

5

Epithelial Chemical Barriers

Epithelial membranes secrete chemicals
-Skin acidity (pH 3-5): ↓bacterial growth
-Sebum & cerumen: toxic to bacteria
-Stomach (pH = 2.0): HCl
-Protein digesting enzymes
-Lysozyme: Saliva & lacrimal fluid
-Mucus: traps microorganisms & dirt

6

Respiratory Tract

Mucus-coated nasal hairs (vibrissae):
-Trap dirt
-Trap microbes
-Trap pollen
-Trap mold spores
Upper respiratory tract:
-Cilia move contaminants trapped in mucus away from the lungs

7

Nonspecific Cells & Chemicals

-Phagocytes
-Natural killer (NK) cells
-Antimicrobial proteins: blood & tissue fluid
-Inflammatory response activates macrophages, WBCs, & chemicals

8

Phagoctyes

Macrophages:
--Free macrophages
Move throughout the body
-Fixed macrophages
Kupffer cells (liver)
Microglia (brain)
Neutrophils:
-Phagocytic for bacteria
Monocytes:
-Phagocytic for bacteria
-Monocytes → macrophages
Eosinophils:
-Phagocytic for parasitic worms

9

Phagocytosis Steps

-Microbe adheres to phagocyte
-Phagocyte pseudopods engulf microbe (antigen) into a phagosome (sac)
-Phagosomes fuse w/ a lysosome to form a phagolysosome
-Microbe inside phagolysosome is digested by enzymes
-Nondigestible material is removed by exocytosis

10

Phagocytosis

SLIDE 12, review the picture

11

Natural Killer (NK) Cells

-Large lymphocytes
-React nonspecifically
-Kill cancer cells
-Kill virus-infected cells
-Kill their target cells by releasing:
-Perforins
-Cytolytic chemicals
-Chemicals ↑inflammatory response

12

Inflammatory Response

-Begins when body tissues are injured
-Prevents the spread of damaging chemicals
-Disposes of cell debris & pathogens
-Sets the stage for repair
-Signs of acute inflammation:
-Redness, heat, swelling & pain

13

Inflammatory Chemicals

-Released by injured tissues & WBCs into cell spaces:
-Prostaglandins
-Complement
-Histamine

14

Vascular Permeability

-Inflammatory chemicals cause:
-↑Capillary wall permeability
-Vasodilation
-Fluid containing plasma proteins & antibodies leaks into the tissue spaces
-Causes edema

15

Vasoconstriction vs. Vasodilation

-Vasoconstriction
-Normal permeability & blood flow
-Vasodilation
-Increased blood flow and permeability of blood vessels with vasodilation

16

Edema

-Accumulation of fluid in the tissue spaces:
-Contributes to sensation of pain
-Dilutes harmful substances
-Brings in ↑oxygen & ↑nutrients (repair)
-Allows entry of clotting proteins to wall-off the infection (prevents bacterial movement)

17

Phagocytic Mobilization Phases (know the definitions)

-Leukocytosis – neutrophils released from bone marrow in response to chemicals released by injured cells
-Margination – neutrophils cling to capillary walls at the injured area
-Diapedesis – neutrophils squeeze through capillary walls
-Chemotaxis – inflammatory chemicals attract neutrophils to the infection site & neutrophils begin phagocytosis

18

Antimicrobial Proteins

-Interferon & complement:
-Enhance nonspecific (innate) defenses
-Attack microorganisms directly
-Prevent microorganism reproduction

19

Interferon

-Interferon synthesis is activated when a cell is invaded by a virus
-Interferon molecules leave infected cell & enter nearby (un-invaded) cells
-Interferon stimulates neighboring cells to activate their genes for antiviral protein production
-Blocks viral reproduction

20

Interferon Action

SLIDE 24, know the picture

21

Interferon Family

-All related immuno-proteins
-WBCs also secrete interferon
-Interferons can activate macrophages & NK cells
-FDA-approved interferon (antiviral drug)
-Used against hepatitis viruses & herpes virus

22

Complement

-Proteins (C1-C9)
-Circulate in blood as inactive proteins
-↑Inflammatory response
-Kill bacteria
-Body cells are immune to complement
-↑Effectiveness of both nonspecific & specific defenses

23

Complement Pathways

-Complement activation:
-Binding of antibodies to invading organisms (antigen)
-Binding of complement to the antigen-antibody complex (complement fixation)
-Activated in a sequence w/ each step catalyzing the next & forms →
-Membrane Attack Complex (MAC)
-Causes cell lysis

24

C-Reactive Protein (CPR)

-Produced (liver) during inflammation
-CPR:
-Targets damaged cells for disposal
-Activates complement
-Used to detect acute infections

25

Fever

-↑Body temperature in response to invading microorganisms
-Body’s thermostat is reset upwards in response to pyrogens
-Pyrogens: chemicals made by WBCs exposed to foreign substances

26

Fever Effects

-High fevers can denature enzymes
-Moderate fevers cause:
-Liver & spleen to store iron (needed by microorganisms)
-↑Metabolic rate → ↑tissue repair

27

Steroid Hormones

-Hydrocortisone, cortisone, cortisol
-↓Inflammation (anti-inflammatory)
-Vasoconstrict: ↓blood flow, ↓edema, ↓redness
-Used clinically to treat inflammatory diseases (rheumatoid arthritis, etc.)
-Side effects: Cushing’s syndrome (↑visceral fat, moon-face, buffalo-hump, ↓memory storage/retrieval)

28

Specific (Adaptive) Defense Systems

-Third line of defense
-Mounts attack against specific foreign substances
-Slower to react than nonspecific (innate) system
-Works with nonspecific (innate) system

29

Specific (Adaptive) Defense (Humoral Immunity)

-B Cells

30

Specific (Adaptive) Defense (Cellular Immunity)

-T Cells

31

Specific (Adaptive) Defense Immune System

-Recognize specific foreign substances (antigens) & has a memory
-Neutralize or destroy foreign substances
-↑Inflammation & activate complement
-Two (overlapping) parts:
-Cellular (cell-mediated) immunity
-Humoral (antibody-mediated) immunity

32

Antigens

-Activate immune system
-Stimulate an immune system
-Large & complex molecules not normally found in the body (non-self)
Molecules found on cells membranes
-Antigens associated with a foreign cell stimulate an immune response

33

Complex Antigens

-Properties:
-Immunogensis:
-↑Lymphocyte production
-↑Antibody production
-Reactivity – react w/ antibodies
-Includes foreign: proteins, nucleic acids, lipids & carbohydrates


34

Incomplete Antigens

-Are not immunogenic
-Are reactive w/ antibodies
-Specific (adaptive) immune system may recognize them as foreign & mount an attack (allergic response)
-Found in:
-Poison ivy, animal dander, dyes, detergents, cosmetics

35

Antigenis Determinants

-Only certain parts of an antigen are immunogenic
-Lymphocytes form antibodies against the antigen
-Antibodies only bind to the antigenic determinants of an antigen
-Naturally occurring antigens have many antigenic determinants

36

Self-Antigens

-Body cells have protein molecules (self-antigens) that are not antigenic to us but are antigenic to other humans
-MHC (Major Histocompatibility Complex) proteins mark a body cell as self

37

MHC Proteins

-Unique to an individual
-Each MHC molecule displays a self-antigen
-In infected cells, MHC proteins bind to fragments of non-self antigens
-MHC proteins play a role in mobilizing the immune system

38

Specific (Adaptive) Immune System

-Lymphocytes:
-T lymphocytes – do not make antibodies (control cellular immunity)
-B lymphocytes – make antibodies (control humoral immunity)
-Antigen-presenting cells (APCs):
-Do not respond to specific antigens
-Play auxiliary roles in immunity

39

Lymphocyte Maturation

-Immature lymphocytes released from bone marrow are all identical
-Whether a lymphocyte becomes a B cell or a T cell depends on where in the body it matures (immunocompetent)
-B cells mature in Bone Marrow
-T cells mature in the Thymus

40

Immunocompetent B or T cells

-Have receptors that respond to specific antigens
-Become immunocompetent before they encounter antigens
-Are exported to lymphoid tissue where they encounter antigens
-Mature into antigen-activated cells upon binding w/ their recognized antigen

41

Lymphocyte Maturation

SLIDE 50, know the picture.

42

Antigen-Presenting Cells (APCs)

-Functions:
-Engulf foreign matter
-Present fragments of antigens on their surfaces to be recognized by T cells
-APCs: macrophages

43

Antigen-Presenting Cells (APCs) Macrophages

-Macrophage engulfs foreign cells
-Attaches foreign antigens (yellow) onto their MHC proteins (green)
-APC presents antigens to Helper T-cells which activate the Helper T-cells

44

Activated Helper T-Cells

Release Chemicals:
-Stimulate macrophages to become activated macrophages
-Activated macrophages secrete bactericidal chemicals

45

Helper T-Cell Function

SLIDE 56, be able to draw and label picture. *ESSAY QUESTION*

46

Cytokines Chemicals (three)

-Chemicals used in cellular immunity:
-Interleukin I
-Interleukin II
-Perforin

47

Cytokines (Interleukin I)

-Produced by macrophages (APC cells)
-Stimulates (activates) Helper T-cells

48

Cytokines (Interleukin II)

-Produced by Helper T-cells
-Stimulates (activates) Cytotoxic T-cells
-Stimulates (activates) B-cells

49

Cytokines (Perforin)

-Produced by cytotoxic T cells
-Causes lysis (punches holes) in target cells membranes

50

Cytotoxic T-Cells (Killer T-Cells)

-Stimulated by Helper T-Cells
-Destroy body cells infected with viruses
-Destroy cancer cells

51

Memory Cells

-T-Cells & B-Cells "remember" an antigen
-React to a second invasion of an antigen more rapidly

52

Regulatory Cells

-Stop T-Cell & B-Cell activity after an infection has been conquered

53

Specific (Adaptive) Immunity: Summary

-Two-part defensive system
-Uses B-lymphocytes, T-lymphocytes & APCs to identify & destroy nonself substances
-Recognizes foreign substances (antigens)
-Cells communicate w/ one another so entire immune system mounts a response specific to those antigens

54

Humoral Immunity Response

-Antigen challenge – 1st encounter between antigens & naive immunocompetent cells
-1st encounter happens in lymphoid organs
-If the lymphocyte is a B-cell:
-Antigen stimulates a humoral immune response
-Antibodies are made against the antigen by the B-cell

55

Clonal Selection

-B-cells form clones with the same antigens specific receptors
-Immuocompetent B-cells activate when antigens bind to their receptors

56

B Cell: Summary

-B-Lymphocytes react directly w/ antigens
-Require stimulation from Helper T-Cells
-Offspring become Plasma Cells & Memory B-Cells
-Humoral Immunity

57

Primary & Secondary Responses

SLIDE 70, know the picture.

58

B Cells Clones

-Most B-cell clones become antibody-secreting plasma cells
-Plasma cells make 2000 antibodies/sec
-Secreted antibodies bind to antigens & mark antigens for destruction
-Some B-cell clones become memory cells
-Memory cells mount an immediate response if future exposures to same antigen occurs

59

Lymphocyte Summary

SLIDE 72.

60

Primary Immune Response

-Primary immune response:
-1st exposure to a specific antigen
-Delay period: 3-6 days after antigen challenge
-Peak levels of antibody are reached in 10 days & then decline

61

Secondary Immune Response

-Secondary immune response: re-exposure to same antigen
-Memory cells respond quickly
-Delay period: hours after antigen challenge
-Antibody levels peak in 2-3 days at higher levels than primary response
-Antibody levels remain high for weeks to months

62

Active Humoral Immunity

-B cells encounter antigens & produce antibodies against the antigens
-Natural Active – response to a bacterial or viral infection
-Artificial Active – response to a vaccine of dead or attenuated pathogens
-Vaccines – spare us the symptoms of a disease
-Weakened antigens provide antigenic determinants & are immunogenic

63

Passive Humoral Immunity

-Differs from active immunity in antibody source & level of protection
-B cells are not challenged by antigens
-Immunological memory does not occur
-Ends when antibodies degrade
-Natural Passive – mother to fetus via placenta
-Artificial Passive – injection of antibodies (gamma globulin)

64

Acquired Immunity- Naturally Acquired

-Active
-Infection; contact with pathogen
-Passive
-Antibodies pass from mother to fetus via placenta; or to infant in her milk

65

Acquired Immunity- Artificially Acquired

-Active
-Vaccine; dead or attenuated pathogens
-Passive
-Injection of immune serum (gamma globulin)

66

Antibodies

-Also called immunoglobulins
-Made by activated B cells & plasma cells in response to an antigen
-Capable of binding only w/ that antigen
-Five classes of antibodies: IgM, IgA, IgD, IgG, IgE (MADGE)

67

Antibody Classes

-IgM: made by plasma cells
-IgA: prevents pathogen attachment to cell surface; in lactiferous secretions (passive immunity)
-IgD: activates B-cells
-IgG: most abundant/diverse antibody; crosses placenta (passive immunity)
-IgE: activate mast cells & basophils to release histamine

68

Basic Antibody Structure

-Antibodies: 4 protein chains
-2 identical Heavy (H) chains
-2 identical Light (L) chains
-Each chain has a constant (C) region at one end
-Each chain has a variable (V) region at the other end
-Variable regions form antigen-binding site

69

Antibody Targets

-Antibodies don’t destroy an antigen (they inactivate it or tag it for destruction)
-Plasma cells can make a billion different antibody types
-Antibody mechanisms: complement fixation/activation, neutralization, agglutination, precipitation

70

Complement Fixation & Activation

-Complement fixation:
-Used against cell antigens
-Antibodies attach to cell (promote cell lysis)
-Complement activation:
-↑Inflammation
-↑Phagocytosis

71

Neutralization

-Neutralization:
-Antibodies block active sites on viruses or bacteria
-Prevents antigens from binding to body cells

72

Agglutination & Precipitation

-Agglutination: antigen-antibody complexes cause clumping
-Precipitation: small soluble molecules → large insoluble complexes

73

Antibody Action

SLIDE 89.

74

Immunodeficiencies

-Function of immune system is abnormal
-Acquired immunodeficiency
-Congenital immunodeficiency

75

Acquired Immunodeficiencies

-Acquired immune deficiency syndrome (AIDS)
-Characteristics:
-Weight loss
-Swollen lymph nodes
-Opportunistic infections occur (pneumonia)

76

AIDS

-Caused by human immunodeficiency virus (HIV) transmitted via body fluids
-HIV enters the body through blood transfusions, contaminated needles, unprotected sex
-Dates back to 1880’s & is descended from a chimpanzee virus in Africa – Nature
-HIV: Destroys helper T cells (↓Cell-mediated immunity)
-HIV multiplies in lymph nodes-no symptoms
-Symptoms: months to years…or never!
-HIV’s surface protein attaches to the CD4 receptor on the helper T cell
-HIV enters the cell
-HIV reverse transcriptase produces DNA from viral RNA
-DNA directs the cell to make new viruses
-Viruses reproduce & infect other cells
-HIV reverse transcriptase is not accurate & produces frequent errors (mutations)
-High mutation rate causes drug resistance
-Treatments:
-Reverse transcriptase inhibitors (AZT)
-Drugs are currently being developed to block HIV’s entry into T-cells (CD4 receptor)


77

Autoimmune Diseases

-Immune system cannot distinguish self from nonself
-Body produces autoantibodies that destroy body tissues
-Examples:
-Multiple Sclerosis, Myasthenia Gravis, Graves’ disease, Lupus, Type I diabetes mellitus, rheumatoid arthritis, glomerulonephritis (Bright’s disease

78

Autoimmune Disease Mechanisms

-New self-antigens appear:
-1) Gene mutations generate new self-antigens
-2) Infectious damage changes original self-antigens
-If determinants on foreign antigens resemble self-antigens:
-Antibodies made against foreign antigens cross-react w/ self-antigens

79

Practical Aspects

-Immune system is impaired by:
-Stress
-Depression
-↓Protein diets
-Sleep deprivation
-With ↑age…the immune system becomes less efficient