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Immunology > Part 2 > Flashcards

Part 2 Flashcards

1
Q

what happens if anatomical barriers fail

A

an infection begins
second line activates

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2
Q

how long does the second line take to activate

A

4 to 96 hours

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3
Q

what happens if the second line fails

A

recruitment of effector cells, PAMPs is recognized, effectors activated, and inflammation.
Moves onto the third line.

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4
Q

how long does it take for the third line to activate

A

96+ hours

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5
Q

how long does the first line take to activate

A

0-4 hours

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6
Q

what is portal of entry

A

the preferred entry a pathogen takes in order to infect the host

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7
Q

how are most pathogens contracted

A

through the mouth and respiratory tract

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8
Q

what are the most common portals of entry

A

Mouth/respiratory tract, GI tract, reproductive tract/other, external surface, wounds/abrasions, insect bites.

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9
Q

what are the features that allow pathogens to evade and penetrate

A

Capsules around the cell wall, usually a sugar layer (anthrax).
Specialized cell walls that allow pathogens to survive harsh environments.
Lysogenic convergence: change outer appearance so IS doesn’t recognize pathogens later.

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10
Q

what kind of cell walls do Gram positive bacteria have

A

thick cell walls

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11
Q

what does being Gram positive do for the bacteria

A

allows it to survive in harsh conditions

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12
Q

what do GPs secrete

A

exotoxins and endotoxins

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13
Q

examples of GP exotoxins

A

A-B exotoxins; superantigens (mounts a super strong immune response; so much so that it can kill you).

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14
Q

examples of GP endotoxins

A

Streptokinase: anti-coagulant

Collagenase: swims through your skin; breaks connective tissue apart (Flesh-eating bacteria).

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15
Q

what features do Gram negative bacteria have

A

a cell membrane, then a thin cell wall, then an outer membrane.

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16
Q

what do GN bacteria secrete

A

endotoxins

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17
Q

examples of GN endotoxins

A

LPS.
LPS is attached to the outer membrane.
Outer membrane is covered in LPS.
LPS acts like an extra layer of protection.

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18
Q

what are the four locations of pathogens

A

Interstitial spaces, blood, and lymph
epithelial surfaces
cytoplasm
vesicles

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19
Q

what are the extracellular locations

A

Interstitial spaces, blood, and lymph
epithelial surfaces

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20
Q

what are the intracellular locations

A

cytoplasm
vesicles

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21
Q

examples of pathogens found in the Interstitial spaces, blood, and lymph

A

Viruses, bacteria, protozoa, fungi, worms.

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22
Q

what is the protective immunity of interstitial spaces, blood, and lymph

A

complement, phagocytosis, antibodies.

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23
Q

examples of pathogens found on epithelial surfaces

A

Worms, gonorrhea, helicobacter pylori

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24
Q

protective immunity of epithelial surfaces

A

Antimicrobial proteins, antibodies (especially IgA)
IgA is found in all secretions: sweat, mucus
IgG is found in blood

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25
Q

pathogens found in cytoplasm

A

Viruses, chlamydia, protozoa

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26
Q

protective immunity of the cytoplasm

A

NKs and cytotoxic T cells (96 days to be fully activated)

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27
Q

pathogens found in vesicles

A

plague, legionnaire’s
Prefer to be in vesicles to evade immune responses.

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28
Q

protective immunity of vesicles

A

T cell and NK dependent macrophage activation.

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29
Q

what does inflammation depend on

A

depends on severity (# of damaged cells)

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30
Q

what is the second line’s intracellular defense mechanism

A

NK cells

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31
Q

what is the second line’s extracellular defense mechanism

A

phagocytic cells

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32
Q

what is the third line’s intracellular defense mechanism

A

CD8 cytotoxic T cells

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33
Q

what is the third line’s extracellular defense mechanism

A

antibodies from the B cells

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34
Q

what does the third line need for both intra and extracellular defense

A

Both require CD4 helper T cells to be activated.

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35
Q

what does the Skin, gut, lungs, eyes/nose/oral cavity all have

A

tight junctions

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36
Q

what are tight junctions

A

proteins that seal the areas between cells.

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37
Q

what are desmosomes

A

like buttons with fibers that anchor cells together.

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38
Q

what are gap junctions

A

openings between the cells, so that cells can share whatever goes through.

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39
Q

what does fungus like in the first defense? what pathogen does it attract?

A

Fungus likes keratin (athletes foot).

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40
Q

what is the mechanical washing of skin and gut

A

longitudinal flow of air and fluid

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41
Q

what is the mechanical washing of lungs

A

movement of mucus by cilia.
Goblet cells

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42
Q

what is the mechanical washing of eyes, nose, mouth

A

tears, nasal cilia.

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43
Q

what chemicals are in the skin

A

fatty acids, B-defensins, lamellar bodies, cathelicidin.
Sebum (fatty acid) prevents hair from becoming brittle.
Sebum is toxic, preventing bacteria from getting in pores/hair follicle.

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44
Q

what chemicals are in the gut

A

low pH, enzymes (pepsin), A-defensins, RegIII, cathelicidin.

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45
Q

what is in the crypt of gut cells

A

A-def and RegIII extremely acidic.
C-type lectins (proteins that bind sugars): RegIII
A-def is amphipathic protein

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46
Q

chemicals in the lungs

A

pulm surfactant, A-def, caths.

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47
Q

chemicals in eyes, nose, mouth

A

enzymes in tears and saliva (lysozyme), histatins, B-defs.

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48
Q

what do all first line components have

A

a microbiota
Bacteria want same bacteria/environments.

49
Q

how do NK cells kill

A

the directed release of lytic granules or by inducing death receptor-mediated apoptosis via the expression of Fas ligand or TRAIL.

50
Q

what is Gram-positive’s thick cell wall is made out of

A

peptidoglycans (NAG and NAM)

51
Q

how are NAG and NAM connected vertically

A

peptide bridges

52
Q

what are the NAG and NAM peptide bridges called

A

B(1,4) glycosidic bond

53
Q

what does lysozyme target

A

B (1, 4) glycosidic bonds

54
Q

what does phospholipase A2 degrade

A

digests phospalipids

55
Q

how do defensins degrade

A

attach to the membrane and create a pore.

56
Q

what are the granules in granulocytes made of

A

filled with defensin proteins (A, B, T)

57
Q

where are alpha defensins found

A

the primary granules

58
Q

what charge are active defensins

A

Cationic is the active portion.

59
Q

what are zymogens

A

proteins that must be cleaved in order to function.

60
Q

what line are antimicrobial proteins found in

A

second line

61
Q

where are complement proteins produced

A

liver

62
Q

what are serine proteases

A

enzymes that cleave peptide bonds in proteins

63
Q

what three complement proteins cause inflammation

A

C3a, C5a, and C5b

64
Q

what does C3 get cleaved to

A

C3a and C3b

65
Q

what is the order in which complement proteins are cleaved

A

C1 > C4 > C2, C3, C4-9

66
Q

what are the four guiding principles of immuno

A

recognition, effector function, regulation, memory

67
Q

what do all complement pathways converge to

A

C3

68
Q

what are effector functions

A

the function of each immunological component
an essential link between innate and adaptive immunity.

69
Q

what are the effector functions of complement proteins

A

Recruit phagocytic cells to infection sites and promote inflammation.
Opsonization to trigger phagocytosis (This is most important)
Apoptosis

70
Q

what is avidity in immuno

A

overall binding strength

70
Q

what is special about mannose

A

is has specific patterns

71
Q

what is affinity in immuno

A

the strength of bonding at one specific site

72
Q

what is the lectin

A

any protein that binds to sugars.

73
Q

how many lectin pathways are there

A

4

74
Q

what are the four lectin paths

A

MBL
Ficolin (M, L, H)

75
Q

what does mbl recognize

A

NAG
Mannose
Fucose

76
Q

characteristics of the mbl monomer

A

3 monomers come together to form a monomer.
Trimeric clusters
A total of 18 binding sites.

77
Q

what does mbl have high avidity to

A

mannose and fucose residues (MASP-2 and MASP-1)

78
Q

how is ficolin different from mbl

A

Different carb-binding domain.

79
Q

what does ficolin recognize

A

NAG (Gram negative and positive)
Teichoic acids (Gram positives)

80
Q

what does ficolin bind to

A

oligosaccharides containing acetylated sugars.

81
Q

what is the first step of lectin pathway

A

Activated MASP 2 (MBL or ficolin) cleaves C4 to C4a (weak trigger of inflammation) and C4b, which binds to the microbial surface.

82
Q

second step of lectin pathway

A

C4b then binds C2, which is cleaved by MASP 2, to C2a and C2b, forming the C4b2a complex.

83
Q

what is a C3 convertase

A

anything that has the potential to cleave C3 to C3a and b.

84
Q

example of C3 convertase in Lectin pathway

A

C4b2a

85
Q

third step of lectin pathway

A

C4b2a cleaves C3 to C3a and b, which binds to the microbial surface or to the convertase itself.

86
Q

fourth step of lectin

A

One molecule of C4b2a can cleave up to 1000 molecules of C3 to C3b. Many C3b molecules bind to the surface of the microbe.

87
Q

where is the newly formed C3 protein bound to in step five

A

thioester bond

88
Q

what is the downside of the thioester bond

A

Thioester is very reactive.
Water can react and turn off the bond to C3.

89
Q

step six of lectin path

A

Cleavage of C3 releases C3a, and a change in conformation of C3b allows the thioester bond to react with a chemical group on the pathogen surface.

90
Q

final step of lectin pathway

A

Thioester bonds on C3b/C4b create covalent bonds on the surface of cells/pathogens.

91
Q

what are the two outcomes of the lectin pathway

A

can result in C3b binding to the pathogen surface

Or C3b is inactivated by hydrolysis (water binds to the thioester bond).

92
Q

what proteins are in the classical pathway

A

C1, 2, 4 3

93
Q

how many C1 proteins are there

A

C1q, r, and s

94
Q

what classical protein is similar to MBL

A

C1q

95
Q

what classical protein is similar to MASP2

A

C1s

96
Q

which classical protein is a serine protease

A

C1s

97
Q

what does C1s cleave to classical

A

C4 and C2

98
Q

what does C4b do classical

A

binds to pathogen and opsonizes it
Binds C2 for cleavage by C1s

99
Q

what does C4a do classical

A

peptide mediator for inflammation

100
Q

what does C2a do classical

A

cleaves C3 and 5

101
Q

what does C2b do classical

A

precursor to vasoactive C2 kinin

102
Q

what does C3b do classical

A

many molecules of c3b bind to the pathogen and act as opsonizers.
unitiate amplification via alt pathway
binds c5 for cleavage by c2b

103
Q

what does c3a do classical

A

peptide mediator for inflammation

104
Q

what is the function of the alternative pathway

A

Makes sure classical and lectin are stronger reactions

105
Q

what are the four main components of alt pathway

A

C3
factors b, d, p

106
Q

first step of alt pathway

A

C3b deposited by classical or lectin pathway C3 convertase.
C3b binds factor B
Bound factor B is cleaved by plasma protease factor D into Ba and Bb.

107
Q

second step of alt path

A

C3bBb (C3 convertase) cleaves many C3 to C3a and C3b.

108
Q

third step of alt path

A

C3 undergoes spontaneous hydrolysis to C3(H2O), which binds to factor B allowing it to be cleaved by factor D to Ba and Bb.
C3(H2O)Bb complex (C3 convertase) cleaves C3 into C3a and b rapidly unless it binds to the cell surface.
Happens in your bloodstream as it isn’t attached to a cell.

109
Q

fourth step of alt path

A

Factor B non covalently binds to C3b on the cell surface and is cleaved into Bb.

110
Q

what is the strongest trigger of inflammation

A

C5a

111
Q

which proteins impact blood vessels to increase vascular permeability and cell-adhesion molecules.

A

C3a, C5a, C4a

112
Q

why is increased permeability of vessels important

A

allows increased fluid leakage from vessels and extravasation of immunoglobulin and complement molecules.
more migration of macros, PMN, and leukocytes

113
Q

what cytokine triggers inflammation

A

TNF alpha and histamine

114
Q

how are holes formed in the membrane for complement system

A

C5 convertase cleaves C5
Converts into C5a and C5b
To C6 to C7 to C8 to C9
C8 has a hydrophobic region, which can interact with the membrane
Wedges itself into the membrane.
C9 binds to polymerize into the MAC, which forms a hole in the membrane.

115
Q

how is the complement system turned off

A

protectin (CD59)

116
Q

How do the 3 pathways carry out effector functions

A

Complement receptors (CRs 1-7)
Macrophages have CRs
Bacterium is coated with C3b
When only C3b binds to CR1, bacteria is NOT phagocytosed.
C5a can activate to phagocytose via CR1.

117
Q
A

Immunology (11 decks)

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