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DMD 5244 (Immunity) > Innate Immunity (complete) > Flashcards

Innate Immunity (complete) Flashcards

1
Q

is innate or adaptive immunity similar in all individuals of a species

A 
innate immunity
(adaptive immunity varies from individual to individual)
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2
Q

is innate or adaptive immunity generally enhanced by repeated exposure

A

adaptive immunity

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3
Q

does innate or adaptive immunity have some sort of “memory”

A

adaptive immunity

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4
Q

does innate or adaptive immunity use nonspecific mechanisms to identify invaders

A

innate immunity

adaptive immunity is based on the recognition or specific invader

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5
Q

are the mechanisms of innate or adaptive immunity mobilized immediately, and work quickly?

A

innate immunity

effector products of adaptive immunity take several days to produce

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6
Q

What happens to the adaptive immune response with each additional exposure to an invader

A

the response becomes quicker, more specific, and is at a higher level.

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7
Q

what are the 6 types of organisms that can grow in vertebrates

A
  1. viruses
  2. bacteria
  3. fungi
  4. parasites
  5. protozoa
  6. worms
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8
Q

What barriers/mechanisms must be overcome by organisms that want to grow in humans

A
  1. Skin
  2. mucous membranes
  3. ciliary escalator in the respiratory tract
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9
Q

which immunity works early in the infection process

A

innate immunity

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10
Q

T/F the adaptive immune response depends on the innate immune response for activation and for most of its effector functions

A

True

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11
Q

why haven’t our bodies adapted and evolved enough over time to already destroy these pathogens

A

because microbes and viruses evolve faster than vertebrates

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12
Q

What are PAMPs

A

pathogen associated molecular patterns.

certain structures that are only found on pathogens

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13
Q

What are some examples of PAMPs

A
  1. double stranded RNA
  2. LPS (lipopolysaccharide)
  3. Lipoteichoic acid
  4. peptidoglycan
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14
Q

on what type of pathogen do you see the PAMP double stranded RNA

A

viruses

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15
Q

on what type of pathogen do you see the PAMP LPS

A

gram negative bacteria

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16
Q

on what type of pathogen do you see lipoteichoic acid

A

the cell wall of gram positive bacteria

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17
Q

on what type of pathogen do you see peptidoglycan

A

the cell wall of gram positive bacteria

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18
Q

what type of immunity focuses on these PAMPs

A

innate immune mechanisms

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19
Q

why don’t these organsims evolve and change their PAMPs so they can’t be used to recognize the organism by immune systems

A

they must be crucial to the organisms and therefor hard to change

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20
Q

What are the three possible immune response outcomes

A
  1. normal response (attacks non-self, leaves self)
  2. immune hyperactivity (allergies, and autoimmunity)
  3. immune hypoactivity (infections, cancer, immunodeficiency)
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21
Q

what are in eyes that are barriers against infection

A

lysozome in tears

washing of the eyes

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22
Q

what acts as barriers on the skin against infection

A
  1. physical barrier

2. antimicrobial secretions

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23
Q

what acts as a barrier in the respiratory system against infection

A
  1. mucus
  2. cilia
  3. alveolar macrophages
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24
Q

What acts as a barrier in the genitourinary tracts against infection

A
  1. low pH of urine
  2. washing of urine
  3. lysozyme
  4. vaginal lactic acid
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25
Q

what acts as a barrier in the digestive tract against infection

A
  1. stomach acidity
  2. normal flora
  3. bile
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26
Q

what are commensals in our body

A

bacteria that live in our body, that aren’t pathogenic.

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27
Q

lysozyme does what, and comes from where?

A

breaks down peptidoglycan

comes from tears, saliva, nasal secretions, body fluids, lysosomal granules

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28
Q

lactoferrin and transferrin do what, and come from where?

A

they bind iron, and compete with microorganisms for it

they come from granules of PMNs

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29
Q

Lactoperoxidase does what, and comes from where?

A

it is inhibitory to many microorganisms

it comes from milk and saliva

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30
Q

B-lysin does what, and comes from where?

A

effective against gram positive bacteria

it comes from thrombocytes and normal serum

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31
Q

Chemotactic factors do what and come from where

A

they induce direct migration of PMNs, monocytes, and other cells
they come from bacteria, products of cell injury, denatured proteins, complement, and cytokines

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32
Q

properdin does what, and comes from where?

A

it activates complement in the absence of the antibody-antigen complex
it is found in normal plasma

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33
Q

cationic peptides do what and come from where

A

they disrupt membranes and block cell-transportation

they come from PMN granules (defensins)

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34
Q

What are the three lines of defense of the immune system. and which are non-specific, and which are specific

A
  1. skin, mucus membranes, chemicals
  2. phagocytosis, complement, interferon, inflammation, fever
  3. lymphocytes and antibodies

1-2 non-specific, 3 - specific

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35
Q

What are the roles of phagocytes in an immune response

A
  1. production of cytokines and chemokines
  2. Ingulf and destroy the pathogen (with out without antibodies)
  3. presentation of antigen fragements to T-cells
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36
Q

which types of phagocytes do the presentation of antigen fragments to T-cells

A

immature dendritic cells, that have been activated by microbial components and cytokines

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37
Q

What happens with the T-cells that have had antigen fragments presented to them by immature dendritic cells

A

they become effector cells, they create an adaptive immune response (present it to B-cells)

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38
Q

What do the cytokines and chemokines secreted by phagocytes do

A
  1. increase vascular dilation
  2. increase vascular permeability
  3. induce production of proteins that recruit more immune cells

= cause inflammation

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39
Q

what does increase vascular dilation and permeability do for an immune response

A

allows more lymphocytes, antibodies, and complement to enter the site of infection

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40
Q

What are antigens

A

molecules that trigger a specific immune response

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41
Q

what are epitopes

A

the portion of the antigen recognized by the antibody or lymphoocyte

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42
Q

how do antigens enter the body

A
  1. through breaks in the skin and mucus membranes
  2. direct injection (bite or needle)
  3. ingestion or inhalation
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43
Q

What is the type of cell from which all cells of the immune system are derived

A

hematopeotic stem cell (HSC)

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44
Q

what does a HSC give rise to each time it divides

A

another HSC and a progenitor cell that is commited to a certain lineage

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45
Q

what are the two lineages of immune cells

A

myeloid (inflammatory cells)

lymphoid (lymphocytes)

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46
Q

which is the only cell that can be formed from both the myeloid and lymphoid lineages

A

dendritic cells

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47
Q

what controls the specific differentiation of progenitor cells

A

hematopoeitins

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48
Q

what cells come through the myeloid lineage

A 
RBCs
platelets
basophils
eosinophils
neutrophils
monocytes (dendritic cells/macrophages)
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49
Q

what cells come through the lymphoid lineage

A

B-cells
T-cells
NK cells (natural killer)

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50
Q

do all cells of myeloid lineage complete differentiation in the same location

A

nope,

bone marrow, peripheral tissues, secondary lymphoid tissue

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51
Q

What are the three types of formed elements in blood

A
  1. RBCs (erythrocytes)
  2. Platelets
  3. WBCs (leukocytes)
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52
Q

What is the function of RBCs

A

carry O2 and CO2 in the blood

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53
Q

what is the function of platelets

A

involved in blood clotting and inflammation

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54
Q

what are the two classes of leukocytes

A

granulocytes

agranulocytes

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55
Q

What are the different types of granulocytes

A

neutrophils
eosinophils
basophils

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56
Q

what are the different types of agranulocytes

A

monocytes

lymphocytes

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57
Q

list the leukocytes from most abundent to least

A 
neutrophils
lymphocytes
monocytes
eosinophils
basophils
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58
Q

what do neutrophils do

A

they are major phagocytes and cause accute inflammation

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59
Q

what do eosinophils do

A

perform parasite defense and regulate inflammation

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60
Q

what do basophils do

A

secrete histamine, involved in allergies

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61
Q

what can high levels of eosinophils in the blood indicate

A

allergies or a parasitic worm infection

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62
Q

what change in white blood cell count does a bacterial infection cause

A

increase in all leukocytes, but mostly neutrophils

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63
Q

what change in white blood cell count does a viral infection cause

A

increase in lymphocytes

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64
Q

what is diapedesis

A

the passages of White blood cells through intact capillaries

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65
Q

what do lymphocytes do

A

they are the main cells in adaptive immune response

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66
Q

what do monocytes do

A

mature into macrophages

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67
Q

what are the phagocytic cells

A

neutrophils
macrophages
dendritic cells

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68
Q

what role do neutrophils play as phagocytes

A

short lived, but quick destructive phagocytosis

release of cytokines = acute inflammation

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69
Q

what roles do macrophages play as phagocytes

A

they are found in various tissues, important in their maintenance and repair
long lived = cells of chronic inflammation
release cytokines

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70
Q

which phagocytes are activated by T-cells and antibodies

A

macrophages

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71
Q

what is phagocytosis

A

a receptor-mediated process whereby large particles are engulfed.

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72
Q

what can the phagocytic receptors bind

A

they can bind microbes directly

they can bind opsonized particles

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73
Q

do some pathogens use phagocytosis to their advantage

A

yes

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74
Q

what are two ways that pathogens can use phagocytosis to their advantage

A
  1. they can get phagocytosed, then rupture the phagosome and enter the cytoplasm
  2. they can block the fusion of lysosomes with the phagosome so they can’t be destroyed
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75
Q

what bacteria rupture the phagosome after they have been phagocytosed and enter the cytoplasm

A

listeria monocytogenes

burkholderia pseudomallei

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76
Q

what bacteria prevent the fusion of the phagosome and lysosome after being phagocytosed

A

mycobaterium tuberculosis

salmonella

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77
Q

what can overcome the block of fusion of the phagosome and lysosome by salmonella and mycobacterium tuberculosis

A

IFN-y (T-cell cytokine)

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78
Q

what are the receptors of macrophages involved in

A
  1. scavenging tissue debris from apoptotic cells
  2. tissue repair and maintenance
  3. production of anti-inflammatory responses
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79
Q

which cells are the phagocytotic cells in the second line of defense

A

macrophages

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80
Q

where do macrophages come from

A

when monocytes leave the blood, they become macrophages in the tissues

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81
Q

what are some names for macrophages that stay in a certain area of the body

A
  1. microglial cells (CNS)
  2. mesangial cells (kidney)
  3. marginal zone (spleen)
  4. Kupffer cells (liver)
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82
Q

are all macrophages fixed to certain tissues

A

nope, some are wandering

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83
Q

are alveolar macrophages fixed, or wandering macrophages

A

wandering

84
Q

what makes up the MPS (mononuclear phagocytotic system)

A

monocytes, macrophages attached to endothelial cells

85
Q

how are microbes killed in a phagocyte

A

they are absorbed and bathed in free radicals, which destroy them

86
Q

what are the different types of dendritic cells

A
  1. immature
  2. mature
  3. follicular
87
Q

what do immature dendritic cells do

A

they phagocytize pathogens, then they become mature

88
Q

what do mature dendritic cells do

A

they present antigens to T-cells

89
Q

what do follicular dendritic cells do

A

present immune complexes to B-cells

90
Q

where are dendritic cells very numerous

A

in epithelia and mucosal surfaces

91
Q

what are langerhans cells

A

specialized dendritic cells in keratinized epidermis that can remain there for months

92
Q

what are dermal or interstitial dendritic cells

A

dendritic cells that reside in the dermal layer

93
Q

what are the different dendritic cells that function in the epithelium of the small intestines

A
  1. some sample gut contents directly
  2. some wait below the epithelial cells to have samples of lumen transported to them
  3. some circulate in the blood and wait for viruses
94
Q

what is the function of the dendritic cells that directly sample the lumen of the small intestine

A

they prevent inflammatory response against the gut commensial bacteria

95
Q

what are the cells that transfer small intestine lumen to lymphoid tissues

A

M-cells

96
Q

what are the dendritic cells called that circulate with the blood and wait for viruses

A

plasmacytoid dendritic cells

97
Q

what do plasmacytoid dendritic cells do when they encounter viruses

A

produce lots of type 1 interferons

98
Q

what are the primary lymphoid organs

A

the locations where lymphocytes mature
Bone marrow
thymus

99
Q

what are secondary lymphoid organs

A 
the locations where antigens are trapped, where an immune response takes place
lymph nodes
spleen
MALT (tonsils)
GALT (peyers patches)
100
Q

what are tertiary lymphoid tissues

A

locations where lymphoid tissues is created at sites of chronic infection

101
Q

what does the spleen do

A

filters for antigens in the blood

102
Q

where do you find the lymphatic tissue (white pulp) of the spleen

A

around arterioles

103
Q

where do you find the marginal zone of the spleen

A

around the white pulp

104
Q

what do you find in the marginal zone of the spleen

A

metallophilic macrophages
marginal zone macrophages
specialized B cells

105
Q

how do antigens get to the GALT

A

they are transported there by M cells

106
Q

what is the first type of cell that the antigens sees in GALT

A

dendritic cells

107
Q

what do sentinal cells do

A

recognize pathogens and secrete cytokines to initiate an immune response

108
Q

can all epithelial cells tolerate microbes on their surface

A

nope, some can, but places like alveoli and small intestines don’t because they would interfere with their function

109
Q

how do the alveoli and small intestines prevent the build up of microbes on their surfaces

A

secreting antimicrobial peptides

defensins and cathelicidins

110
Q

what are defensins

A

small antimicrobial peptides with a 3 stranded beta-sheet and 3 disulfide bonds

111
Q

what are cathelicidins

A

they are small antimicrobial peptides, but differ from defensins in structure (a-helical regions)

112
Q

what are the types of defensins

A

alpha and beta

113
Q

how do alpha and beta defensins differ

A

both come from neutrophils, but beta can come from epithelia too
both are antimicrobial, but beta are chemotactic, and induce histamine release

114
Q

what are the paneth cells of the small intestine

A

cells that produces alpha defensins in response to bacteria

115
Q

what do the a-defensins of paneth cells destroy

A

giardia, but only one of them (cryptdin-3) kills E. coli

116
Q

how do defensins kill microbes

A
  1. they bind to the acidic phospholipids in the membranes of microbes
  2. they enter the membranes and create pores
  3. this causes the cells to lyse
117
Q

how do some bacteria combat the pore creation in their membranes by defensins

A

they modify their membrane lipids with lysine = reduction of negative charge = insensitive

118
Q

what are collectins and ficolins

A

soluble proteins at mucosal surfaces or in blood that recognize carb configurations on microbes.

119
Q

what are the structures of collectins

A

they are a long chain, with a big carb recognizing head

120
Q

what do collectins do

A

the head binds to a sugar on the microbe, this increases phagocytosis, and activates complement

121
Q

what is the complement system

A

a series of about 30 proteins that can be activated in 3 ways

122
Q

what happens in the activation of the 30 proteins in the complement system

A

proteins are cleaved into two substances
beta - stays
alpha - leaves

123
Q

what are the three pathways in activation of the complement system

A

lectin pathway
classical pathway
alternative pathway

124
Q

what are the four ends of the complement system

A
  1. lysis of bacteria
  2. chemotaxis of phagocytes to the bacteria
  3. opsonization of bacteria
  4. all of which increase inflammation
125
Q

what are the two main players in the lectin pathway of the complement system

A

MBL

ficolins

126
Q

what are the three main players in the classical pathway of the complement system

A

IgG, IgM, pentraxins

127
Q

what is the main player in the alternative pathway of the complement system

A

microbial membranes

128
Q

the early events of all three pathways of the complement system all lead to what

A

the cleavage of C3 by C3 convertase

129
Q

which complements lead to inflammation, chemoattraction

A

C3a

C5a

130
Q

which complements lead to induction of phagocytosis

A

C3b

131
Q

which complements lead to attack on membranes

A

C5b, C6, C7, C8, C9

132
Q

which complements lead to promotion of antibody production

A

C3b

133
Q

which complements are the late events

A

C5-C9

134
Q

how is the classical pathway of the complement system activated

A
  1. C1q/r/s complex couples with pentraxins or antibodies
  2. C1s cleaves C4
  3. C4b binds to cell surface
  4. C2 binds to C4b
  5. C1 cleaves C2
  6. C4b-C2b = C3 convertase
  7. C3 convertase cleaves = C3a, C3b
135
Q

how is the lecthin pathway of the complement system activated

A
  1. MBL or ficolin bind to the microbial surface carbs
  2. MASP’s bind to MBL/Ficolin
  3. MASP2 cleaves C4
  4. C4b stays attached
  5. C2 binds to C4b
  6. C2 is cleaved by MASP-2
  7. C4b-C2b = C3 convertase
  8. C3 convertase cleaves = C3a, C3b
136
Q

how is the alternative pathway of the complement system activated

A
  1. C3a and C3b bind to the cell surface
  2. B binds to C3b
  3. D cleaves B
  4. C3b-Bb = C3 convertase
  5. C3 convertase cleaves = C3b, C3a
137
Q

what happens to C3b that can’t find a microbe to bind to

A

it is bound by factor H, then factor I cleaves the C3b (making it inactive)

138
Q

what does properdin do in the complement pathways

A

it stabilizes the C3b/Bb complex

139
Q

what happens when C3b attaches to either the C3b/Bb or C4b/C2b complexes

A

this leads to the cleavage of C5

140
Q

what does C5a do

A

it is a proinflammatory peptide that acts on endothelial cells and mast cells.
it is a powerful neutrophil chemoattractant

141
Q

what does C5b do

A

it nucleates the formation of the (MAC) membrane attack complex (this makes large holes in the cell)

142
Q

defects in which components of the complement can cause SLE (systemic lupus erythematosis)

A

defects in C1 and C4

143
Q

how do defects in C1 and C4 lead to SLE (systemic lupus erythematosis)

A

they lack the ability to clear apoptotic cell debris and immune complexes

144
Q

the deficiency of which complement component is the most severs

A

C3

145
Q

what do defects in the late part (C5-C9) cause

A

severe nisseria infections

146
Q

how do microbes fight against the actions of the complement system

A
  1. make surface proteins that bind factor H (so that it will inactivate C3b)
  2. make proteins that bind to C4bp (an inactivator of C4b)
  3. take host control proteins with them as they bud
147
Q

what microbes make surface proteins that bind factor H to fight against the complement system

A 
HIV
S. Pyogenes
S. Pneumonia
Neisseria
B. Burgdorferi
gonorrhoeae
148
Q

which microbes make proteins that bind C4bp to fight against the complement system

A

gonorrhoeae

B. pertussis

149
Q

which microbes take host control proteins with them as they Bud

A

HIV-1

vaccina

150
Q

which fuse first, primary or secondary granulues

A

secondary (yep these fuse first)

151
Q

what does NAPDH oxidase create

A 
O2
H2O2
HOCl
OH
ONOO (with NO from iNOS)
152
Q

what does iNOS create

A

NO

ONOO (with O2 from NAPDH oxidase)

153
Q

which attack first, the toxic O2 intermediates or the toxic nitrogen intermediates

A

the toxic O2 intermediates are used immediately, the toxic nitrogen intermediates are used later, and last longer

154
Q

what happens when you have defects in any subunit of the NADPH oxidase

A

you will get a chronic granulomatus disease (CGD)

patients have a hard time clearing infections and get persisting granulomas

155
Q

What are the three types of sentinel immune cells in tissues

A
  1. macrophages
  2. Mast cells
  3. immature dendritic cells
156
Q

what do sentinel immune cells do

A

recognize microbial threats and initiate an inflammatory immune response.

157
Q

what do sentinel cells have to differentiate between

A

apoptotic bodies and microbial threats

158
Q

what allows sentinel cells to distinguish between apoptotic bodies and microbial threats

A

TLRs (toll like receptors)

159
Q

what are TLRs (toll-like receptors)

A

a protein with an extracellular portion with lots of leucine (LRRs) a transmembrane domain, and a Toll/IL-1 receptor (TIR) domain

160
Q

what can TLRs bind

A

Nucleic acids
Proteins
Lipids
polysaccharides

161
Q

are accessory proteins sometimes used to help things bind to TLRs

A

yes

162
Q

how do sentinel cells recognize LPS

A
  1. LPS is taken from the cell wall by LBP
  2. LBP gives the LPS to CD14
  3. CD14 give the LPS to TLR/MD-2 complex
  4. this sends a signal into the cell
163
Q

what is required for LPS responsiveness of TLR4

A

MD-2

164
Q

is CD14 required for LPS response

A

no, but it helps a lot

165
Q

where do you find TLRs that recognize microbial cell wall components

A

in the plasma memebrane

166
Q

where do you find TLRs that recognize microbial nucleic acids

A

in the intracellular membranes (phagosomes or endosomes)

167
Q

What does the Activation of TLRs lead to

A

production of cytokines
TNF
IFN (alpha and beta)
IL (6 and 12)

168
Q

what do NOD1, NOD2 and Cryopyrin do

A

recognize parts of peptidoglycan, and activate NF-kB (inflammatory cytokine)

169
Q

when TLRS and sentinel cells recognize microbes, what do they do

A

release cytokines
release chemokines
release lipid mediators

these lead to a coordinated response by vessels and leukocytes = inflammation

170
Q

what are the 4 main functions of inflammation mediators

A
  1. increase vascular permeability
  2. change adhesive properties of the epithelium (increased amounts of leukocytes)
  3. activate phagocytes
  4. activate NK cells
171
Q

what are the two proteolytic cascades triggered by activation of endothelial cells

A

kinin cascade

coagulation cascade

172
Q

how does the kinin cascade affect inflammation

A

increases vas. permeability

173
Q

how does the coagulation cascade affect inflammation

A

clotting reactions decrease microbial spread

174
Q

Where does TNF come from

A

macrophages and mast cells

175
Q

what does TNF do

A 
increases: 
vascular permeability
endothelial cell adhesiveness
activation of phagocytes
cytoxicity of NKcells
176
Q

what does IL-1 come from

A

macrophages, mast cells, KC, EC

177
Q

What does IL-1 do

A

increases chemokine production and endothelial cell adhesiveness

178
Q

Where does IL-6 come from

A

macrophages, mast cells, FB

179
Q

what does IL-6 do

A

recruites monocytes, systemic effects

180
Q

what does IL-12 come from

A

macrophages

181
Q

what does IL-12 do

A

increases IFN-y production by NK cells

increases NK cytoxicity

182
Q

what does IFN-y come from

A

NK cells

183
Q

what does IFN-y do

A

enhances phagocytosis and killing by phagocytes

184
Q

what do chemokines come from

A

macrophages, mast cells, EC

185
Q

what do chemokines do

A

attract neurtophils. monocytes, effector T-cells

186
Q

what are the antinflammatory cytokines

A

IL-10 and TGF-Beta

187
Q

how does arachadonic acid turn into inflammatory mediators

A
  1. a stimulus activates PLA2 and COX-2
  2. PLA2 pulls arachadonic acid from phospholipids
  3. COX-2 breaks arachadonic acid into PGH2
  4. PGH2 is broken down into PGI, PGE, PGF, and thromboxane
188
Q

what are luekotrienes involved in

A

chronic inflammation

189
Q

what are the steps in getting neutrophils out of the blood and into the tissues

A

rolling
activation
adhesion
diapedesis

190
Q

what cells dominate acute inflammation

A

neutrophils

191
Q

what cells dominate chronic inflammation

A

macrophages and Tcells

192
Q

What mediates the shift from acute inflammation to chronic inflammation

A

IL-6

193
Q

what effects to proinflammatory cytokines systemically

A
  1. TNF uses fat and muscle cells to mobilize energy stores
  2. IL-1 and IL-6 sitmulate the liver to produce proteins to help fight infection
  3. IL-1 and IL-6 act on the hypothalamus to induce a fever
194
Q

what is the acute phase response

A

when IL1 and IL6 stimulate the liver to produce proteins that help fight infection

195
Q

what are antiinflammtory actions

A
  1. glucocorticoids
  2. IL10 and TGF-b
  3. acetylcholine receptors
196
Q

What are the two types of interferons

A 
type 1 (IFN -a and IFN-b) 
type 2 (IFN-y)
197
Q

what is type 1 interferon

A

IFNa and IFNb
they are produced by infected cells, and by cells sensing viruses through TLR.
they work against virus’s
they leave the infected cells and go to nearby cells. they stop the cells from proliferating the virus

198
Q

what is type 2 interferon

A

they are antiviral and antibacterial (IFN-y)

199
Q

what does type 1 interferon do to cells

A
  1. through PKR they shut off all translation
  2. degrade RNA
  3. inhibit transcription
200
Q

what does type 2 interferon do to cells

A

shut off all translation through PKR

201
Q

what cells produce Interferons

A

macrophages, immature dendritic cells, plasmacytoid dendritic cells

202
Q

which cells produce the most interferons

A

plasmacytoid dendritic cells

203
Q

what TLR gives rise to IFN-B

A

TLR 3

204
Q

what TLD gives rise to IFN-a

A

TLR 7,8,9

205
Q

what is the most potent activator of macrophages

A

IFN-y

DMD 5244 (Immunity) (16 decks)

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