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OLD "MIC 660" > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What are the 4 types of pathogens?

A
  1. bacteria
  2. viruses
  3. fungi
  4. parasites
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2
Q

What are 2 examples of the first line of defense?

A
  1. physical barriers
  2. mucous membranes
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3
Q

What are 4 examples of the second line of defense?

A
  1. phagocytic leukocytes
  2. antimicrobial proteins
  3. inflammation
  4. fever
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4
Q

What are 3 examples of the third line of defense?

A
  1. lymphocytes
  2. antibodies
  3. memory cells
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5
Q

What are granulocytes and what do they do?

A

cells that contain granules
involved in innate immunity

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6
Q

What are agranulocytes and what do they do?

A

cells that DONT contain granules
differentiate into B, T, NK, dendritic and macrophages

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7
Q

What 4 things does the innate immune system do?

A
  1. pattern recognition
  2. antimicrobial proteins
  3. inflammation
  4. fever
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8
Q

What is pattern recognition?

A

soluble proteins tag pathogens so receptors on innate cells can recognize them so NK cells or phagocytes can destroy them

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9
Q

What is the 2 benefits of a fever?

A
  1. lower replication of pathogen
  2. increases activity of adaptive immunity
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10
Q

What is an antigen?

A

substance that can stimulate an immune response

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11
Q

Are B or T cell involved in Humoral immunity?

A

B cells

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12
Q

Are B or T cell involved in Cell-Mediated immunity?

A

T cells

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13
Q

Do B or T cells present antigens on MHC molecules?

A

B cells

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14
Q

Do B or T cells recognize antigens presented on MHC molecules?

A

T cells

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15
Q

What do cytotoxic T cells do?

A

directly target and kill infected cells

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16
Q

What is clonal selection and expansion?

A

selection: T cells with receptors that recognize the specific pathogen are activated
expansion: T cell that can recognize the specific pathogen is proliferated

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17
Q

What is the difference between the intensity of the first exposure to pathogen v. the second exposure?

A

more intense and quicker (more antibody affinity)

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18
Q

What are 2 examples of primary lymphoid tissue and what happens there?

A
  1. bone marrow (B cells)
  2. Thymus (T cells)
    cell maturation
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19
Q

What are 5 examples of primary lymphoid tissue and what happens there?

A
  1. lymph nodes
  2. tonsils
  3. spleen
  4. Peyer’s patch
  5. MALT
    site for presenting antigens and lymphocyte activation
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20
Q

What type of secondary lymph tissue has no inflammation?

A

MALT

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21
Q

What is hypersensitivity?

A

immune reaction to something that is not a threat to the body (allergies)

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22
Q

What is autoimmunity?

A

disease driven by an immune response against self-antigen due to failure to eliminate auto reactive B/T cells

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23
Q

What is immunodeficiency?

A

lack of immune system function

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24
Q

What is the difference between primary and secondary immunodeficiency?

A

primary - inherited
secondary - aquired

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25
Q

What 4 ways can the immune system go wrong?

A
  1. autoimmunity
  2. hypersensitivity
  3. cancer
  4. immunodeficiency
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26
Q

What is an example of physical barriers?

A
  1. skin
  2. mucosal surfaces
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27
Q

What is an example of a organelle that contains antimicrobial protein and how does it work?

A

lysosome
cleaves polysaccharide of bacterial cell wall

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28
Q

How do antimicrobial proteins disrupt pathogen membranes?

A

their positive charge allows insertion into pathogen

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29
Q

How do cells of the innate immune system detect the presence of pathogens?

A

pattern recognition receptors

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30
Q

What do pattern recognition receptors recognize?

A

PAMPs

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31
Q

What are 5 examples of PRR?

A
  1. Toll-like receptors
  2. lectins
  3. scavenger receptors
  4. cytosolic innate receptor
  5. opsonin receptor
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32
Q

How do toll-like receptors work?
What do they bind to and what do they induce?

A

PAMPs bind to TLR inducing production of cytokines

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33
Q

How do Lectin receptors work?

What do they bind to and what do they induce?

A

bind to carbohydrates (glycans) on pathogens inducing phagocytosis

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34
Q

How do scavenger receptors work?
What do they bind to and what do they induce?

A

recognize negativity charged PAMPs inducing phagocytosis

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35
Q

How do cytosolic innate receptors work?
What do they bind to and what do they induce?

A

recognize intracellular PAMPs then inhibit pathogen growth and recruit WBC

Located cytosol

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36
Q

How do opsonic receptors work?
What do they bind to and what do they induce?

A

tag pathogens with opsonin as a target for phagocytosis

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37
Q

What are 2 examples of opsonic receptors?

A

Fc and CR1

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38
Q

Lectin, scavenger, and opsonin receptors are located ___________ and induce __________

A

innate cell surface
phagocytosis

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39
Q

TLRs and cytosolic innate receptors induce ____________ which signals _________

A

signaling pathways
cytokines

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40
Q

What are the 3 phagocytic cells?

A
  1. macrophages
  2. neutrophils
  3. dendritic cells
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41
Q

What is the first responding immune cell?

A

neutrophils

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42
Q

What is the purpose of cytokines?

A

“sound the alarm”
communicate among the immune cells

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43
Q

What are the 2 types of cytokines?

A
  1. inflammatory
  2. antiviral
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44
Q

What do inflammatory cytokines do?

A

stimulate inflammation at site of infection

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45
Q

What do antiviral cytokines do?

A

limit viral replication and activate NK cells

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46
Q

What is an example of antiviral cytokines?

A

alpha / beta INF

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47
Q

What are chemokines?

A

secreted proteins within the cytokine family who induce migration of WBC

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48
Q

What are the 4 major cells of the innate immune system?

A
  1. macrophages
  2. NK cells
  3. neutrophils
  4. dendritic cells
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49
Q

What is the function of macrophages?

A

phagocytosis and production of inflammatory cytokines via PRR signaling

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50
Q

What is the function of neutrophils?

A

granulocyte that kills pathogens

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51
Q

What 3 ways can neutrophils kill pathogens?

A
  1. phagocytosis
  2. degranulation
  3. NETosis
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52
Q

What is the most numerous WBC?

A

neutrophils

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53
Q

What is the primary component of pus?

A

neutrophils

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54
Q

What is neutrophil migration?

A

process that gets neutrophils to the site of infection

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55
Q

What are the 4 adhesion molecules in neutrophil migration?

A
  1. glycoproteins
  2. integrin
  3. selectins
  4. immunoglobulin-like molecule
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56
Q

What are the 4 steps of neutrophil migration?

A
  1. rolling adhesion
  2. tight binding
  3. diapedsis
  4. migration
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57
Q

Describe the process of neutrophil migration?

A
  1. weak integration between selectins and glycoproteins allow neutrophils to slowly roll on endothelia surface
  2. IL-B and TNF-a (inflammatory cytokines) induce expression of binding integrins
  3. neutrophils move in between cells
  4. gradient directs neutrophils to infection
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58
Q

what are 2 examples of inflammatory cytokines?

A
  1. IL-1B
  2. TNF-a
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59
Q

What is the function of dendritic cells?

A

present peptides on MHC to T cells in lymphoid tissue

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60
Q

What is the function of NK cells?

A

kill cells infected with intracellular pathogens by making holes in the cell membrane

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61
Q

Cytokine INF-a/b induces NK cell proliferation via _________ signaling?

A

paracrine

62
Q

Cytokine INF-a/b alter the expression of receptors on the infected cell that signal NK cells via ___________ signaling?

A

autocrine

63
Q

NK cells also secret INF-g that recruits _____________

A

cytotoxic T cells

64
Q

What is complement fixation?

A

attachment of proteins to pathogens marking them as non-self for phagocytosis

65
Q

How does MAC kill microbes?

A

forms holes in extracelluar pathogens

66
Q

What is an anaphylatoxin?

A

complement protein fragments that induce inflammation

67
Q

What are the 3 complement pathways?

A
  1. alternative
  2. lectin
  3. classical
68
Q

In all complement pathways, what is the key step?

A

cleavage of C3 into C3a and C3b

69
Q

What is the order of activation of the complement pathways?

A
  1. alternative
  2. lectin
  3. classical
70
Q

What does Factor B do in the alternative complement pathway?

A

binds to C3 and is cleaved by Factor D leaving Bb bound to C3

71
Q

What does Factor D do in the alternative complement pathway?

A

cleaves Factor B into Bb (connected to C3)

72
Q

Describe C3a and C3b

A

C3a: soluble anaphylatoxin
C3b: thioester bond that binds to pathogens

73
Q

What happens to C3b when no pathogen is present?

A

remains soluble and is inactive

74
Q

What happens in the alternative pathway once C3b binds to a pathogen’s surface?

A

more Factor B is bound then cleaved by Factor D creating the alternative C3 convertase

75
Q

What is the alternative pathway C3 convertase?

A

C3bBb

76
Q

How does opsonization occur in the complement system?

A

C3b binds to pathogen which is recognized by phagocytes CR1 (receptor) inducing phagocytosis

77
Q

What are 2 methods of C3b regulation via PLAMA PROTEINS?

A
  1. Properdin (Factor P)
  2. Factor H and I
78
Q

How does Properdin (Factor P) regulate C3b?

A

protects alternative C3 convertase on pathogen surface so it can cleave into C3b

79
Q

How does Factor H and I regulate C3b?

A

cleaves bound C3b making it inactive

80
Q

What are 2 methods of C3b regulation via MEMBRANE PROTEINS?

A
  1. Decay Accelerating Factor (DAF)
  2. Membrane Cofactor Protein (MCP)
81
Q

How does Decay Accelerating Factor (DAF) regulate C3b?

A

disassembles alternative C3 convertase on human cells

82
Q

How does Membrane Cofactor Protein (MCP) regulate C3b?

A

disassembles alternative C3 convertase and promotes Factor I (inactivation of C3b)

83
Q

How is the C5 convertase of the alternative pathway made?

A

C3b binds to the C3 convertase C3bBb3b

84
Q

What is the alternative C5 convertase?

A

C3bBb3b

85
Q

__________ is cleaved into ______ which goes onto initiate the MAC

A

C5 convertase; C5b

86
Q

Explain the building of the MAC?

A
  1. C5b, C6, C7 bind
  2. C7 hydrophobic site inserts into pathogen membrane
  3. C8 binds to unit allow C9 to bind and bore hole
87
Q

How do PLASMA PROTEINS regulate MAC?

A

prevent C6 and C7 from associating with human cells

88
Q

How do CELL-SURFACE PROTEIN regulate MAC?

A

prevent C9 recruitment on human cells

89
Q

What are 2 examples of anaphylatoxins in the complement pathway?

A

C3a
C5a

90
Q

What 3 places do anaphylatoxins bind after the complement pathway and why?

A
  1. Endothelial cells (increase vascular permeability)
  2. granulocytes (degranulation)
  3. phagocytes (attractant)
91
Q

What 2 pathways in complement require acute phase inflammation to activate?

A

lectin and classical
(proteins required are not always in circulation)

92
Q

______ causes liver cells to change proteins they secret leading to production of mannose-binding lectin and C-reactive protein

A

IL-6

93
Q

What does MBL do in the lectin pathway?

A

binds to mannose on pathogens

94
Q

What does MASP-1 & 2 do in the lectin pathway?

A

cleaves C4 and C2

95
Q

What does C4b do in the lectin pathway?

A

binds to pathogen’s surface with thioester bond (similar to C3b)

96
Q

What does C2b do in the lectin pathway?

A

binds to C4b (similar to Factor B) making the lectin C3 convertase

97
Q

What is the C3 convertase of lectin pathway?

A

C4bC2b

98
Q

What does C-reactive protein (CRP) do in the classical pathway?

A

binds to phosphocholine on pathogens via C1

99
Q

What are the 3 complex of C1 in the classical pathway?

A

C1r
C1s
C1q

100
Q

What do each of the C1 complexes do in the classical pathway?

A

C1q: binds to CRP and activates C1s and C1r
C1s: cleaves C4 and C2 to generate the classical C3 convertase

101
Q

What is the C3 convertase of the classical pathway?

A

C4bC2b

102
Q

How is C3b and C3a made for each complement pathway?

A

C3 convertase of each pathway is cleaved creating C3a and C3b

103
Q

What do protease inhibitors do and what is an example?

A

inhibit bacterial proteases
a2-macroglobulin: traps protease like a trap

104
Q

What do 3 things do defensins do?

A
  1. poke holes in microbe membranes
  2. neutralize toxins
  3. chemoattractants
105
Q

What tissues express a-defensins?

A

neutrophils and Paneth cells

106
Q

What tissues express B-defensins?

A

epithelial cells, respiratory, and urogenital track

107
Q

What is the difference between primary and secondary immunodeficiencies?

A

primary: inherited
secondary: aquired

108
Q

The type of organism helps identify the __________ in an immunodeficiency

A

defect/mutation

109
Q

What are the 5 categories of innate immunodeficiencies?

A
  1. physical/microbial
  2. complement
  3. PRR/cytokine
  4. phagocytic
  5. NK cells
110
Q

What are 2 examples of physical/microbial immunodeficiencies?

A
  1. Cystic Fibrosis
  2. Crohn’s Disease
111
Q

What are 3 examples of complement immunodeficiencies?

A
  1. regulatory proteins (Factor H&I)
  2. MAC deficiency
  3. HANES
112
Q

What is an example of PRR/cytokine immunodeficiency?

A

recurrent HSE (herpes)

113
Q

What are 3 examples of phagocytic immunodeficiencies?

A
  1. Leukocyte adhesion deficiency (LAD)
  2. Chediak-Higashi syndrome (CHS)
  3. Chronic granulomatous disease (CGD)
114
Q

What are 2 examples of NK cell immunodeficiencies?

A
  1. classical
  2. functional
115
Q

How is Cystic Fibrosis an immunodeficiency?

A

CFTR is mutated causes thick sticky mucus causing biofilms that prevent immune cells and antibiotics

116
Q

How is Crohn’s Disease an immunodeficiency?

A

Paneth cells lack a-defensins causing increased microflora

117
Q

How is loss of Factor H and I an immunodeficiency?

A

Factor H and I down regulate complement by inactivating C3b

so if they’re missing C3 is depleted in serum causing increased bacterial infections

118
Q

How is improper formation of MAC an immunodeficiency?

A

defects in any subunit of MAC causes recurrent infections

119
Q

How is HANE (complement) an immunodeficiency?

A

Loss of C1INH (C1 inhibitor) leads to non specific cleavage of C4 and C2 causing unwanted inflammation that doesn’t respond to meds

120
Q

What is pyogenic bacteria?

A

induces neutrophilic inflammation and pus

121
Q

How is recurrent HSE an immunodeficiency?

A

TRAF3 (induces INF-a/b antiviral cytokine) expression is decreased causing increased viral replication and decreased NK cells activation

122
Q

How is leukocyte adhesion deficiency (LAD) an immunodeficiency?

A

defect in B2-integrin affects tight binding because LFA-1 which induced tight binding of neutrophils on the surface of epithelial cells is defective

no opsonization and phagocytosis

recurrent skin and muscoa infections

123
Q

How is Chediak-Higashi Syndrome (CHS) an immunodeficiency? And what’s made because of this

A

inability to merge lysosome and phagosome because of giant granules and defective NK cells

recurrent bacterial infections that phagocytes normally can control

124
Q

How is Chronic Granulomatous Disease (CGD) an immunodeficiency? And what is caused by the deficiency?

A

NADH does not produce superoxide and hydrogen peroxide to lower pH

no break down

build up of neutrophils

recurrent bacterial and fungal infections

125
Q

How is classical NK cell deficiency an immunodeficiency?

A

absence or very low numbers of NK cells

126
Q

How is functional NK cell deficiency an immunodeficiency?

A

Fc-gamma receptor on NK cells that participate in ADCC (interaction of NK cells with infected cell surface receptors) are mutated

no cytotoxic granules released

127
Q

What is antibody dependent cell-mediated cytotoxicity (ADCC)?

A

Fc-gamma receptors on NK cells engage antibody-bound infected cells and induce death via cytotoxic granules

128
Q

What is the purpose of antimicrobial peptides?

A

Form pores in cells

129
Q

What are mast cells important for?

A

Inflammation

130
Q

NK cells don’t recognize PAMPs, What do they recognize on infected cells?

A

Receptors that are meant to be inactive. If they are activated on the infected cell the NK cell will kill the host cell

131
Q

What does histamine cause?

A

Swelling

132
Q

What causes the heat from a fever?

A

Increased metabolism

133
Q

Antibodies are easier to deal with intra or extracellular pathogens?

A

Extracellular

134
Q

Where does the colonel process occur?

A

Secondary lymph tissue

135
Q

What occurs in the lymph nodes?

A

Dendritic cell presentation and cleaning on lymphatic fluid

136
Q

What allows transportation in MALT since no inflammation can occur here?

A

M cells

137
Q

What is inside lysosomes that destroy pathogens?

A

Antimicrobial peptides

138
Q

What cell cleans up neutrophils?

A

Macrophages

139
Q

What signals the release of mannose binding lectin and c reactive protein in the liver?

A

IL-6

140
Q

What cells do antiviral cytokines signal for?

A

NK cells

141
Q

What kind of TLRs target Intracellular pathogens by looking for viral DNA and RNA?

A

Endosomal TLRs

142
Q

Where are TLRs located for extracellular pathogens?

A

Cell surface

143
Q

What are the only PRR that are not located on cell surface?

A

Cytosol-innate receptors
Endosomal TLRs

144
Q

What cell type is important for Intracellular pathogens?

A

NK cells

145
Q

What does iC3b bind to?

A

CR3 and CR4

146
Q

C4 and C2 are involved in what 2 pathways?

A

Classical
Lectin

147
Q

What is LFA-1 important for?

A

Tight binding of neutrophils

148
Q

What is selectin important for?

A

Rolling adhesion of neutrophils

149
Q

What is LFA-1 important for?

A

Tight binding of neutrophils

150
Q

What happens if NK cells are deficient in FC-gamma?

A

Cannot do ADCC

151
Q

What introduced the expression of integrins for tight binding in neutrophil migration?

A

IL-B
TNF-a
(Inflammatory cytokines)

OLD "MIC 660" (10 decks)

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