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Flashcards in Immunology I Deck (129):
1

Define immunity

resistance to disease

2

What are the two intrinsic systems of the immune system?

innate (nonspecific) and adaptive (specific) defense system

3

What is included in innate defenses?

skin, mucous membranes, phagocytes, fever, NK cells, antimicrobial proteins, inflammation

4

What is included in the adaptive defenses?

humoral (b cells) and cellular (t cells) immunity

5

What is the first line of defense of innate immunity?

skin and mucosa

6

What is the second line of defense of innate immunity?

antimicrobial proteins, phagocytes

7

What does the second line of defense of the innate immune system do?

inhibits spread of invaders. inflammation is most important mechanism

8

What is the third line of defense?

adaptive system. attacks foreign substances. takes longer to react than innate

9

What are some of the protective chemicals of the surface barriers?

skin acidity, lipids in sebum, dermcidin in sweat, HCl in stomach, lysozyme in saliva/lacrimal fluid, mucus

10

What are some of the modifications of the respiratory system involved with innate defenses?

mucus-coated hairs in nose, cilia of upper respiratory tract sweep dust/bacteria up

11

What are the internal defenses of the innate immune system?

phagocytes, NK cells, inflammatory response, antimicrobial proteins (interferon/complement), fever

12

Describe macrophages

develop from monocytes to become main phagocytic cell. free macrophages wander thru tissues, fixed macrophages are permanent residents of some organs

13

What is an example of a free macrophage?

alveolar macrophages

14

What is an example of a fixed macrophage?

kupffer cells

15

Describe neutrophils

become phagocytic on encountering infectious mat'l in tissues

16

What is the first step of phagocytosis?

adherence of phagocyte to pathogen

17

How is the first step of phagocytosis facilitated?

by opsonziation-coating of pathogen by complement or antibodies

18

What is the second step of phagocytosis?

phagocyte forms pseudopods that engulf the particles forming phagosome

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What is the third step of phagocytosis?

lysosome fuses with phagocytic vesicle, forming a phagolysosome

20

What is the fourth step of phagocytosis?

lysosomal enzymes digest the particles, leaving a residual body

21

What is the fifth step of phagocytosis?

exocytosis of the vesicle removes indigestible and residual matl

22

What are the steps for phagocyte mobilization?

leukocytosis, margination, diapedesis, chemotaxis

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Leukocytosis

release of neutrophils from bone marrow in response to leukocytosis-inducing factors from injured cells

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margination

neutrophils cling to the walls of capillaries in the inflamed area

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chemotaxis

inflammatory chemicals (chemotactic agent) promote positive chemotaxis of neutrophils

26

diapedesis

neutrophils flatten and squeeze out of capillaries

27

What are the different mechanisms that destroy pathogens by phagocytosis ?

acidification and digestion by lysosomal enzymes, respiratory burst, oxidizing chemicals

28

respiratory burst

release of cell-killing free radicals, activations of additional enzymes

29

Describe NK cells and what they do?

large granular lymphocytes. target cells that lack self receptors. induce apoptosis in cancer/virus cells. secrete potent chemicals that enhance inflammation

30

When is the inflammatory response activated?

Triggered whenever body tissues are injured or infected

31

How does the inflammatory response help the body?

prevents the spread of damaging agents, disposes of cell debris and pathogens, sets the stage for repair

32

What are the cardinal signs of acute inflammation?

redness, heat, swelling, pain (and sometimes impairment of fxn)

33

Describe the role of TLRs in inflammation?

macrophages and epithelial cells of boundary tissues have TLRs. Activated TLRs trigger the release of cytokines that promote inflammation

34

What are the different inflammatory mediators?

histamine, blood proteins, kinins, prostaglandins, leukrotrienes, and complement

35

What releases kinins, PGs, leukotrienes, and complement?

injured tissue, phagocytes, lymphocytes, basophils, and mast cells

36

How does inflammation and vasodilation relate?

inflammatory chemicals cause dilation of arterioles and increased permeability of local capillaries--->edema

37

What does exudate contain?

proteins, clotting factors, antibodies

38

What is the fxn of exudate?

moves foreign mat'l into lymph vessels, delivers clotting proteins to form a scaffold for repair and to isolate the area

39

What is the fxn of interferons and complement proteins?

attack microorganisms directly and reduce its ability to reproduce

40

Explain how interferon works with virus infected cells

viral-infected cells are activated to secrete IFNs. IFNs enter neighboring cells. Neighboring cells produce antiviral proteins that block viral reproduction

41

What are the fxns of IFNs?

anti-viral, reduce inflammation, activate macrophages and mobilize NK cells

42

What are genetically engineered IFNs used for?

antiviral agents against hepatitis and genital warts. MS treatment

43

What does complement do?

major mechanism for destroying foreign substances, amplifies inflammatory response, kills cells by lysis, enhances both nonspecific and specific defenses

44

Describe the classical pathway of complement activation

antibodies bind to invading organisms. C1 binds to the antigen-antibody complexes (complement fixation)

45

Describe the alternative pathway of complement activation

triggered when activated C3, B,D, and P interact on the surface of microorganisms

46

Where do both pathways of complement activation converge?

converge on C3 which cleaves into C3a and C3b

47

How does complement cause cell lysis?

C3b initiates formation of a membrane attack complex. MAC causes cell lysis by inducing a massive influx of water.

48

What else does C3b do besides initiate formation of MAC?

causes opsonization

49

What does C3a do?

causes inflammation

50

What are the benefits of moderate fever?

causes the liver and spleen to sequester Fe and Zn and increases BMR speeding up repair

51

Why are high fevers dangerous?

heat denatures proteins

52

How is fever initiated?

leukocytes and macrophages exposed to foreign substances secrete pyrogens. pyrogens reset the body's thermostat

53

Antigens

substances that can mobilize the adaptive defenses and provoke immune response. large, complex molecules not normally found in body

54

What are important fxnal properties of complete antigens?

immunogenicity and reactivity

55

Immunogenicity

ability to stimulate proliferation of specific lymphocytes and antibodies

56

Reactivity

ability to react with products of activated lymphocytes and antibodies released

57

What are some examples of complete antigens?

foreign protein, polysaccharides, lipids, nucleic acids

58

What are haptens (incomplete antigens)?

small molecules (peptides, nucleotides, hormones), immunogenic when attached to body proteins, cause an immune system to mount a harmful attack

59

What are some example of haptens?

poison ivy, animal dander, detergents, cosmetics

60

What are antigenic determinants and what is their fxn?

certain parts of an entire antigen that are immunogenic. antibodies and lymphocytes bind to them

61

What are self-antigens?

protein molecules on the surface of cells that are antigenic to others in transfusions or grafts. MHC proteins

62

What are MHC proteins?

coded for by genes of the major histocompatibility complex and are unique to the individual

63

Class I MHC proteins

found on virtually all body cells

64

Class II MHC proteins

found on certain cells in the immune response

65

What do MHC proteins do?

display peptides (usually self-antigens). in infected cells, they display fragments of foreign antigens

66

What do antigen presenting cells do?

do not respond to specific antigens. play essential auxiliary roles in immunity

67

Where do B cells mature?

Red bone marrow

68

Where do T cells mature?

thymus

69

What is immunocompetence?

the ability to recognize and bind to a specific antigen

70

What is self-tolerance?

unresponsiveness to self antigens

71

Describe positive selection of T cells

selects T cells capable of binding to self MHC proteins

72

Describe negative selection of T cells

prompts apoptosis of T cells that bind to self-antigens displayed by self-MHC. ensures self-tolerance

73

What happens to self-reactive B cells?

are eliminated by apoptosis (clonal deletion), undergo receptor editing, and are inactivated if they escape bone marrow

74

How is antigen receptor diversity determined?

genes determine which foreign substances the immune system will recognize and resist

75

What is the fxn of APCs?

engulf antigens, present fragments of antigens to T cells

76

What are the major types of APCs?

dendritic cells, macrophages, B cells

77

What do activated T cells do to macrophages?

turn them into insatiable phagocytes and tell them to secrete bactericidal chemicals

78

Why are dendritic cells unique as APCs?

They are the only ones who have the ability to induce a primary immune response in naive T cells

79

What critical fxns do dentritic cells perform?

critical in the establishment of memory and maintenance of B cell fxn

80

What is the antigen challenge and where does it occur?

It's the first encounter btw an antigen and a naive immunocompetent lymphocyte. usually occurs in the spleen or lymph node

81

What is the fxn of most clone cells?

become plasma cells that secrete specific antibodies

82

What happens to clone cells that don't become plasma cells?

become memory cells. provide memory and mount immediate response to future exposures of the same antigen

83

Describe primary immune response.

occurs on the first exposure to a specific antigen. lag period of 3-6 days. peak levels of plasma antibody are reached in 10 days. antibody levels then decline

84

Describe secondary immune response

occurs on re-exposure to the same antigen. sensitized memory cells respond within hrs. Antibody levels peak in 2-3 days at higher levels. antibodies bind with greater affinity. antibody level can remain high for weeks to months

85

When does active humoral immunity occur?

when B cells encounter antigens and produce specific antibodies against them

86

Describe naturally acquired active immunity?

response to a bacterial or viral infection

87

Describe artificially acquired active immunity?

response to a vaccine of dead or attenuated pathogens

88

What is the fxn of vaccines?

provide antigenic determinants that are immunogenic and reactive.

89

Why do vaccines fail to fully establish immunological memory?

because they target only one type of helper T cell

90

Describe passive humoral immunity

B cells are not challenged by antigens, immunological memory doesn't occur

91

Describe naturally acquired passive immunity?

antibodies delivered to a fetus via the placenta or to infant thru milk

92

Describe artificially acquired passive immunity

injection of serum such as gamma globulin. protection is immediate but ends when antibodies degrade

93

What are immunoglobulins?

the gamma globulin portion of blood

94

What are antibodies?

proteins secreted by plasma cells that are capable of binding specifically with antigen detected by B cells

95

Describe the basic antibody structure

T or Y shaped. Two heavy and two light chains. Variable region is where antigen binds

96

What does the constant region of antibodies determine?

the antibody class (MADGE), the cells and chemicals that the antibody can bind to, how the antibody class fxns in antigen eliminations

97

Describe IgM

first class released during primary response. potente agglutinating agent. fixes and activates complement

98

Describe IgA

found in body secretions. helps prevent attachment of pathogens to epithelial cell surfaces

99

Describe IgD

attached to external surface of B cell. fxn as antigen receptor of B cells

100

Describe IgG

most abundant antibody. Protects against bacteria, viruses, toxins. Fixes complement. Main antibody in secondary and late primary response. Provides passive immunity to fetus

101

Describe IgE

secreted in skin, mucosa of GI and respiratory, tonsils. Binds to mast cells and basophils. When activated causes cells to release histamine that mediate inflammation and allergic rxn. fights parasites

102

What are the defense mechanisms used by antibodies?

neutralization, agglutination, precipitation, complement fixation

103

describe neutralization

antibodies block specific sites on pathogens. prevent these antigens from binding to tissue cells. antigen-antibody complexes undergo phagocytosis

104

describe agglutination

antibodies bind the same determinant on more than one cell bound antigen. cross-linked antigen-antibody complexes agglutinate

105

describe precipitation

soluble molecules are cross-linked. complexes precipitate and are subject to phagocytosis

106

What is the main antibody defense against cellular antigens?

complement fixation and activation

107

What are monoclonal antibodies?

commercially prepared pure antibody. produced by hybridomas (fusion of tumor cell and B cell)

108

What is the use of monoclonal antibodies?

proliferate indefinately and have the ability to produces a single type of antibody. used in research, clinical testing, and cancer treatment

109

What are the targets of the humoral response?

bacteria and molecules in extracellular environments

110

What are the targets of the cell-mediated response?

body cells infected by viruses/bacteria, abnormal or cancerous cells, cells of infused or transplanted foreign tissue

111

Which MHC proteins do CD4 cells bind to?

II MHC

112

Which MHC proteins do CD8 cells bind to?

class I MHC

113

How do dendritic cells obtain other cell's endogenous antigens?

engulfing dying virus-infected or tumor cells, or by importing antigens thru temporary gap jxns w/infected cells

114

Describe the role of antigen binding in T cell activation

antigen binding stimulates the T cell, but co-stimulation is required before proliferation can occur

115

What is co-stimulation?

required T cell binding to other surface receptors on an APC

116

What triggers proliferation and differentiation of activated T cell?

cytokines (IL-1/2 from APCs or T cells)

117

What happens to T cells without co-stimulation?

become tolerant to that antigen, are unable to divide, don't secrete cytokines

118

What happens to T cells that are activated?

enlarge, proliferate, and form clones. differentiate and perform fxns according to their T cell class

119

What is a crucial co-stimulatory signal for T cell activation?

B7 binding with CD28 receptor on a T cell

120

What is a B7 protein?

B7 proteins are produced on the surface of dendritic cells and macrophages when innate defenses are mobilized

121

Why is T cell apoptosis important after immune response has peaked?

activated T cells are a hazard

122

What is the fxn of cytokines?

mediate cell development, differentiation, and responses in the immune system

123

What two classes do cytokines include?

interleukins and interferons

124

Describe the fxn of IL-1

released by macrophages, co-stimulates bound T cells

125

Describe the fxn of IL-2

key growth factor, acts on cells that release it and other T cells

126

What is the role of Helper T cells?

once primed by APC antigen, they help activate T and B cells, induce T and B cell proliferation, activate macrophages and recruit other immune cells

127

What is the role of cytotoxic T cells?

directly attack and kill other cells.

128

What is the role of NK cells?

recognize lack of class I MHC, antibody coating a target cell, different surface marker on stressed cells.

129

What is the role of regulatory T cells?

dampen the immune response by direct contact or by inhibitory cytokines. important in preventing autoimmune rxns