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Immunology > Immunology I > Flashcards

Immunology I Flashcards

1
Q

Define immunity

A

resistance to disease

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2
Q

What are the two intrinsic systems of the immune system?

A

innate (nonspecific) and adaptive (specific) defense system

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3
Q

What is included in innate defenses?

A

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

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4
Q

What is included in the adaptive defenses?

A

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

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5
Q

What is the first line of defense of innate immunity?

A

skin and mucosa

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6
Q

What is the second line of defense of innate immunity?

A

antimicrobial proteins, phagocytes

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7
Q

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

A

inhibits spread of invaders. inflammation is most important mechanism

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8
Q

What is the third line of defense?

A

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

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9
Q

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

A

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

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10
Q

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

A

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

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11
Q

What are the internal defenses of the innate immune system?

A

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

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12
Q

Describe macrophages

A

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

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13
Q

What is an example of a free macrophage?

A

alveolar macrophages

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14
Q

What is an example of a fixed macrophage?

A

kupffer cells

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15
Q

Describe neutrophils

A

become phagocytic on encountering infectious mat’l in tissues

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16
Q

What is the first step of phagocytosis?

A

adherence of phagocyte to pathogen

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17
Q

How is the first step of phagocytosis facilitated?

A

by opsonziation-coating of pathogen by complement or antibodies

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18
Q

What is the second step of phagocytosis?

A

phagocyte forms pseudopods that engulf the particles forming phagosome

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19
Q

What is the third step of phagocytosis?

A

lysosome fuses with phagocytic vesicle, forming a phagolysosome

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20
Q

What is the fourth step of phagocytosis?

A

lysosomal enzymes digest the particles, leaving a residual body

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21
Q

What is the fifth step of phagocytosis?

A

exocytosis of the vesicle removes indigestible and residual matl

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22
Q

What are the steps for phagocyte mobilization?

A

leukocytosis, margination, diapedesis, chemotaxis

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23
Q

Leukocytosis

A

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

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24
Q

margination

A

neutrophils cling to the walls of capillaries in the inflamed area

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25
Q

chemotaxis

A

inflammatory chemicals (chemotactic agent) promote positive chemotaxis of neutrophils

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26
Q

diapedesis

A

neutrophils flatten and squeeze out of capillaries

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27
Q

What are the different mechanisms that destroy pathogens by phagocytosis ?

A

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

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28
Q

respiratory burst

A

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

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29
Q

Describe NK cells and what they do?

A

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

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30
Q

When is the inflammatory response activated?

A

Triggered whenever body tissues are injured or infected

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31
Q

How does the inflammatory response help the body?

A

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

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32
Q

What are the cardinal signs of acute inflammation?

A

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

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33
Q

Describe the role of TLRs in inflammation?

A

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

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34
Q

What are the different inflammatory mediators?

A

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

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35
Q

What releases kinins, PGs, leukotrienes, and complement?

A

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

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36
Q

How does inflammation and vasodilation relate?

A

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

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37
Q

What does exudate contain?

A

proteins, clotting factors, antibodies

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38
Q

What is the fxn of exudate?

A

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

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39
Q

What is the fxn of interferons and complement proteins?

A

attack microorganisms directly and reduce its ability to reproduce

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40
Q

Explain how interferon works with virus infected cells

A

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

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41
Q

What are the fxns of IFNs?

A

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

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42
Q

What are genetically engineered IFNs used for?

A

antiviral agents against hepatitis and genital warts. MS treatment

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43
Q

What does complement do?

A

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

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44
Q

Describe the classical pathway of complement activation

A

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

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45
Q

Describe the alternative pathway of complement activation

A

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

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46
Q

Where do both pathways of complement activation converge?

A

converge on C3 which cleaves into C3a and C3b

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47
Q

How does complement cause cell lysis?

A

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

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48
Q

What else does C3b do besides initiate formation of MAC?

A

causes opsonization

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49
Q

What does C3a do?

A

causes inflammation

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50
Q

What are the benefits of moderate fever?

A

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

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51
Q

Why are high fevers dangerous?

A

heat denatures proteins

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52
Q

How is fever initiated?

A

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

53
Q

Antigens

A

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

54
Q

What are important fxnal properties of complete antigens?

A

immunogenicity and reactivity

55
Q

Immunogenicity

A

ability to stimulate proliferation of specific lymphocytes and antibodies

56
Q

Reactivity

A

ability to react with products of activated lymphocytes and antibodies released

57
Q

What are some examples of complete antigens?

A

foreign protein, polysaccharides, lipids, nucleic acids

58
Q

What are haptens (incomplete antigens)?

A

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

59
Q

What are some example of haptens?

A

poison ivy, animal dander, detergents, cosmetics

60
Q

What are antigenic determinants and what is their fxn?

A

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

61
Q

What are self-antigens?

A

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

62
Q

What are MHC proteins?

A

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

63
Q

Class I MHC proteins

A

found on virtually all body cells

64
Q

Class II MHC proteins

A

found on certain cells in the immune response

65
Q

What do MHC proteins do?

A

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

66
Q

What do antigen presenting cells do?

A

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

67
Q

Where do B cells mature?

A

Red bone marrow

68
Q

Where do T cells mature?

A

thymus

69
Q

What is immunocompetence?

A

the ability to recognize and bind to a specific antigen

70
Q

What is self-tolerance?

A

unresponsiveness to self antigens

71
Q

Describe positive selection of T cells

A

selects T cells capable of binding to self MHC proteins

72
Q

Describe negative selection of T cells

A

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

73
Q

What happens to self-reactive B cells?

A

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

74
Q

How is antigen receptor diversity determined?

A

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

75
Q

What is the fxn of APCs?

A

engulf antigens, present fragments of antigens to T cells

76
Q

What are the major types of APCs?

A

dendritic cells, macrophages, B cells

77
Q

What do activated T cells do to macrophages?

A

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

78
Q

Why are dendritic cells unique as APCs?

A

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

79
Q

What critical fxns do dentritic cells perform?

A

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

80
Q

What is the antigen challenge and where does it occur?

A

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

81
Q

What is the fxn of most clone cells?

A

become plasma cells that secrete specific antibodies

82
Q

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

A

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

83
Q

Describe primary immune response.

A

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
Q

Describe secondary immune response

A

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
Q

When does active humoral immunity occur?

A

when B cells encounter antigens and produce specific antibodies against them

86
Q

Describe naturally acquired active immunity?

A

response to a bacterial or viral infection

87
Q

Describe artificially acquired active immunity?

A

response to a vaccine of dead or attenuated pathogens

88
Q

What is the fxn of vaccines?

A

provide antigenic determinants that are immunogenic and reactive.

89
Q

Why do vaccines fail to fully establish immunological memory?

A

because they target only one type of helper T cell

90
Q

Describe passive humoral immunity

A

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

91
Q

Describe naturally acquired passive immunity?

A

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

92
Q

Describe artificially acquired passive immunity

A

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

93
Q

What are immunoglobulins?

A

the gamma globulin portion of blood

94
Q

What are antibodies?

A

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

95
Q

Describe the basic antibody structure

A

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

96
Q

What does the constant region of antibodies determine?

A

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

97
Q

Describe IgM

A

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

98
Q

Describe IgA

A

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

99
Q

Describe IgD

A

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

100
Q

Describe IgG

A

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

101
Q

Describe IgE

A

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
Q

What are the defense mechanisms used by antibodies?

A

neutralization, agglutination, precipitation, complement fixation

103
Q

describe neutralization

A

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

104
Q

describe agglutination

A

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

105
Q

describe precipitation

A

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

106
Q

What is the main antibody defense against cellular antigens?

A

complement fixation and activation

107
Q

What are monoclonal antibodies?

A

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

108
Q

What is the use of monoclonal antibodies?

A

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

109
Q

What are the targets of the humoral response?

A

bacteria and molecules in extracellular environments

110
Q

What are the targets of the cell-mediated response?

A

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

111
Q

Which MHC proteins do CD4 cells bind to?

A

II MHC

112
Q

Which MHC proteins do CD8 cells bind to?

A

class I MHC

113
Q

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

A

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

114
Q

Describe the role of antigen binding in T cell activation

A

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

115
Q

What is co-stimulation?

A

required T cell binding to other surface receptors on an APC

116
Q

What triggers proliferation and differentiation of activated T cell?

A

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

117
Q

What happens to T cells without co-stimulation?

A

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

118
Q

What happens to T cells that are activated?

A

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

119
Q

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

A

B7 binding with CD28 receptor on a T cell

120
Q

What is a B7 protein?

A

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

121
Q

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

A

activated T cells are a hazard

122
Q

What is the fxn of cytokines?

A

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

123
Q

What two classes do cytokines include?

A

interleukins and interferons

124
Q

Describe the fxn of IL-1

A

released by macrophages, co-stimulates bound T cells

125
Q

Describe the fxn of IL-2

A

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

126
Q

What is the role of Helper T cells?

A

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
Q

What is the role of cytotoxic T cells?

A

directly attack and kill other cells.

128
Q

What is the role of NK cells?

A

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

129
Q

What is the role of regulatory T cells?

A

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

Immunology (8 decks)

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