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PMCOL 303 > immunotoxicology > Flashcards

immunotoxicology Flashcards

1
Q

what are 3 immune mechanisms that are modulated by xenobiotics

A

immune cell activation
immunosuppression
immune recognition

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2
Q

what is immunotoxicity

A

the study of adverse effects on the immune system resulting from exposure to drugs or chemicals

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3
Q

what are the 2 components of the immune system

A

innate and adaptive

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4
Q

what are the 4 types of cells that come from common lymphoid progenitor

A

NK B T and dendritic cells

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5
Q

what are the 6 types of cells that come from common granulocyte/macrophage progenitor

A

eosinophil, basophil, macrophage, neutrophil, mast cell and dendritic cell

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6
Q

what is the cellular components of the innate immune system

A

macrophages, dendritic cells, granulocytes, mast cells, NK cells

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7
Q

what is the cellular components of the adaotive immune system

A

T cells B cells

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8
Q

what is the efferent mechanisms of the innate immune system (4)

A

cytokine production, inflammatory response, phagocytosis, pathogen killing

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9
Q

what is the efferent mechanisms of the adaptive immune system (3)

A

antibody production, cytokine production, cell killing

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10
Q

how fast is the innate response

A

quick

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11
Q

how fast is the adaptive response

A

slow

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12
Q

does innate have specific memory

A

no

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13
Q

does adaptive have specific memory

A

yes

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14
Q

what is the main important differences between innate and adaptive (2)

A

antibody formation and immune memory

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15
Q

where are macrophages

A

in tissues (only called macrophages when there)

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16
Q

what are kupffer cells

A

resident macrophages in the liver

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17
Q

what is the largest macrophage population in the body

A

kupffer cells

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18
Q

what do kupffer cells do main mechanism

A

remove foreign material from portal circulation that streams into liver

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19
Q

what is a secondary mechanism of kupffer cells

A

synthesize and release proinflammatory mediators like cytokines, ROS, RNS

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20
Q

what is the main enzyme of macrophages

A

using NADPH oxidase

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21
Q

what do macrophages produce

A

NO

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22
Q

what do macrophages release (2)

A

proteases and cytokines

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23
Q

what cytokines do macrophages release (3)

A

TNFa, IL-1B and IL-18

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24
Q

what does cytokine release from macrophages do

A

signal for neutrophil recruitment

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25
Q

what are the 2 waves of attack in hepatic cells

A
  • macrophage catalyzed

- neutrophil catalyzed

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26
Q

why do neutrophils come in wave 2

A

because cytokine signals tell them do

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27
Q

how do neutrophils fight in wave 2

A

indiscriminately, even will damage host tissue

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28
Q

what is an example of toxicity of a xenobiotic that macrophages play a role in

A

CCl4

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29
Q

what happens do CCl4 in the body

A

CYP2E1 turns it into *CCl3

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30
Q

what happens when you deplete macrophages and then give CCl4

A

there is less liver injury, so it is protective

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31
Q

how did they get rid of macrophages to test for CCl4 effects

A

give them GdCl3 cause it depletes macrophages

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32
Q

what happens if you give GdCl3 and CCl4 + why

A

then there wont be any injury (no macrophages to cause more damage)

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33
Q

what 2 pathways can happen to *CCl3

A

-add O2 to make *OOCCl3 -add lipid to make lipid radical and CHCl3

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34
Q

what are 2 drugs that the depletion of macrophages attenuates the toxic effects

A

acetaminophen and CCl4

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35
Q

what is immunosuppression

A

impairment of maturation and development of immune cells

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36
Q

what is a main example of something used for immunosuppression (xeno)

A

halogenated aromatic hydrocarbons

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37
Q

what is pancytopenia

A

low rbc wbc and platelets

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38
Q

what are 4 causes of immune suppression

A

xenobiotic-induced, panytopenia (bone marrow), thymic atrophy/involution
tumor

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39
Q

what is thymic atrophy/involution / what happens (5)

A

less T cells being made, less proliferation differentiation cytokine production and cell responses

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40
Q

what is TCDD (another name)

A

dioxin

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41
Q

what does dioxin do

A

decreases thymus mass

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42
Q

what does TCDD do

A

decreases thymus mass

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43
Q

which drugs decreases thymus mass

A

TCDD/dioxin

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44
Q

what happens if you give dioxin then influenza A

A

they get more pulmonary damage than mice who werent exposed

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45
Q

what does dioxin do to T cells (4)

A

t-cell depletion, less t-cell differentiation and proliferation
but more regulatory T cells

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46
Q

what does AhR stand for

A

aryl hydrocarbon receptor

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47
Q

where is the aryl hydrocarbon receptor

A

in the cytosol

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48
Q

where is there a lot of aryl hydrocarbon receptor

A

in the thymus

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49
Q

what happens with aryl hydrocarbon receptor knockout

A

the mice are resistant to thymic atrophy caused by TCDD/ dioxin

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50
Q

what does TCDD need to activate for it to cause a bad response

A

the aryl hydrocarbon receptor

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51
Q

what does trp depletion cause

A

T cell death

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52
Q

what does trp breakdown into

A

kynurenine

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53
Q

what do tumor cells upregulate

A

enzymes that breakdown trp

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54
Q

what does kynurenine do

A

binds to aryl hydrocarbon receptor

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55
Q

what happens when kynurenine binds to aryl hydrocarbon receptor (3)

A

induces IL-10 release and regulatory T cell development which leads to immune suppresion

56
Q

what is the role of regulatory T cells

A

role in regulating or suppressing other cells in the immune system

57
Q

what does more regulatory T cells lead to (2)

A

less T cell proliferation, less killer t cell formation

58
Q

how does trp depletion lead to immunosuppression in cancer

A

tumor cells upregulate enzymes to turn it into kynurenine, which binds to aryl hydrocarbon receptor to increase IL-10 and T regulatory cells

59
Q

what is type 1 hypersensitivity

A

immediate-type hypersensitivity

60
Q

what is type 2 hypersensitivity

A

antibody mediated cytotoxic hypersensitivity

61
Q

what is type 3 hypersensitivity

A

immune complex mediated hypersensitivity

62
Q

what is type 4 hypersensitivity

A

cell mediated hypersensitivity

63
Q

which type of hypersensitivity is anaphylaxic

A

type 1

64
Q

what are the 2 fragments of the IgG molecule

A

the Fc and the Fab fragments

65
Q

is the Fc or Fab fragment the one that looks like the two ends sticking out from 1

A

Fab

66
Q

is the Fc or Fab fragment the one that looks like main one that 2 things brach from

A

Fc

67
Q

which fragments only has constant regions

A

Fc

68
Q

which fragments has variable and constant regions

A

Fab

69
Q

which one is the heavy and light chain

A

heavy is on the outer one and light is the inner one

70
Q

where are the variable regions

A

right at the end of the Fab fragments

71
Q

what part of IgG binds to the antigen

A

the variable region on Fab

72
Q

what part of IgG activates complement and phagocytes

A

Fc

73
Q

what is the main type of antibody we are learning about

A

IgG

74
Q

which side is the amino terminal of IgG

A

the Fab regions

75
Q

which side is the carboxy terminal of IgG

A

the Fc regions

76
Q

which type of populations get lots of type 1 hypersensitivity

A

in developed nations

77
Q

what is a prerequisite of type 1 hypersensitivity

A

need prior sensitization to antigen (so you have antibodies the second time)

78
Q

what is the specific antigen in type 1 hypersensitivity

A

IgE

79
Q

what specifically happens in type 1 hypersensitivity

A

binding of antigen to antigen specific IgE bound on mast cells, then rapid liberation of active chemicals such as histamine

80
Q

what do mast release once activated

A

active chemicals such as histamine

81
Q

what happens in type 1 hypersensitivity when they are first exposed to the antigen

A

they make IgE antibodies, they bind to surfaces of mast cells and basophils(by Fc portion), and these cells are now primed to react the next time the cells come into close proximity with the allergen

82
Q

how does IgE bind to mast cells

A

by its Fc portion onto a Fc receptor for IgE (which is already on the mast cell)

83
Q

how does degranulation occur in type 1 hypersensitivity

A

exposure to antigen causes cross-linking of cell-bound IgEs, so then degranulation happens

84
Q

which cell type is sensory and decides what is foreign

A

the B cell

85
Q

what does the B cell do once it notices a foreign thing

A

processes it, presents it to T cell

86
Q

which cell type secreted IgE

A

plasma cells

87
Q

what are 2 examples of primary mediates in degranulation in type 1 hypersensitivity + what do they . cause

A

histamine, proteases

can cause vasodilation

88
Q

what are 2 examples of secondary mediates in degranulation in type 1 hypersensitivity + what do they . cause

A

leukotrienes and prostaglandins

89
Q

what is the mechanism of antihistamines

A

block H1 and H2 receptors

90
Q

what is the mechanism of cromolyn sodium

A

blocks Ca++ influx into mast cells

91
Q

what is the mechanism of theophylline

A

prolongs high cAMP in mast cells by inhibiting phosphodiesterase

92
Q

what is the mechanism of ephinephrine

A

stimulates cAMP production in mast cells

93
Q

what is the mechanism of cortisone

A

blocks histidine to histamine conversion and stimulates cAMP in mast cells

94
Q

why do lots of drugs to treat type 1 increase cAMP

A

because degranulation is prevented if cAMP levels remain high

95
Q

what happens in type 2

A

specific IgG or IgM antibodies bind to antigens on cells via their Fab regions

96
Q

what happens once the IgG binds to the cell in type 2

A

complement activation via Fc region

97
Q

what does complement activation cause (type 2)

A

attracts phagocytes, causes damage and lysis

98
Q

how does IgG cause complement (type 2)

A

bridges complement via Fc regions

99
Q

what are 3 examples of complement mediated lysis in type 2

A

hemolytic anemia, ABO transfusion, Rh disease

100
Q

what are the antigens in type 2

A

it can be part of the cell naturally, or a drug!

101
Q

what are 2 examples of drugs that can be used as antibodies in type 2

A

penicillin, quinidine

102
Q

what is opsonization

A

coating of a particle with proteins that facilitate phagocytosis (targets and tags the cell)

103
Q

which type of hypersensitivity involves opsonization

A

type 2

104
Q

which type of hypersensitivity involves IgE

A

type 1

105
Q

which type of hypersensitivity involves mast cell

A

type 1

106
Q

which type of hypersensitivity involves cell bound antigen

A

type 2

107
Q

which type of hypersensitivity involves immune complex

A

type 3

108
Q

what is the first step of type 3 hypersensitivity

A

antigen and antibodies form complexes in blood

109
Q

what happens to the immune complexes

A

they are deposited on blood vessels wall

110
Q

what happens once the immune complexes are deposited on blood vessels wall

A

complement is activated and C3a and C5a are released

111
Q

what happens once C3a and C5a are released

A

neutrophils are attracted by C5a, they release enzymes that destroy endothelium and RBC escape the vessels

112
Q

what do neutrophils do it type 3 and how do they come around

A

attracted by C5a and they release enzymes that destroy endothelium and RBC escape the vessels (inflammation, leaky vessels)

113
Q

what does procainamide do (which type)

A

lupus like syndrome (type 3)

114
Q

what is the mechanism of procainamide in type 3 + what does it cause

A

forms anti H2A-H2B-DNA antibodies which causes abnormal T cell maturation and proliferation

115
Q

how does procainamide cause T cell activation

A

because its reactive metabolite activates T cells

116
Q

what does procainamide do to T cells

A

abnormal T cell maturation, proliferation, T cell activation

117
Q

what is a main serious thing that procainamide can cause (1 word)

A

agranulocytosis

118
Q

what is agranulocytosis

A

lowered WBC count

119
Q

which type causes agranulocytosis

A

3

120
Q

what kind of antibodies does procainamide make

A

against histones and DNA (H2A-H2B-DNA)

121
Q

which type of hypersensitivity is T-cell mediated

A

4

122
Q

what is the first thing that happens in class 4

A

macrophages ingests antigen, processes it, and presents it with class 2 MHC protein

123
Q

what happens after macrophage presents antigen with MHC 2

A

T helper-1 gets activated, gabba-INF, activates macrophages

124
Q

what are some things that may be involved with class 4

A

CD4 and CD8 cells

125
Q

what is involved with poison oak, ivy, drugs, soaps and heavy metals

A

CD8 cell is involved (type 4)

126
Q

what can CD4 cells do

A

delayed-type hypersensitivity and immune inflammation: induce cytokines and recruit neutrophils, inflammation

127
Q

what can CD8 cells do

A

cell mediated cytolysis: granzymes, express Fas ligant - both apoptosis

128
Q

what are granzymes

A

proteases that induce apoptosis

129
Q

what are the 3 main components of type 4

A

macrophage (APC)
MHC class 2
helper t cells

130
Q

what cell type has CD4

A

helper t cells

131
Q

what cell type has CD8

A

killer t cells

132
Q

can xenobiotics activate the immune system

A

yes

133
Q

can xenobiotics suppress the immune system

A

yes

134
Q

are immune activation mechanisms simple + explain

A

no they are simple and can involve various types of hypersensitivity reactions or direct cytotoxic mehcanisms

135
Q

what are 2 things that immunosuppression primarily efects

A

the thymus (via AhR) and the bone marrow

PMCOL 303 (25 decks)

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