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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
pathogens found in cytoplasm
Viruses, chlamydia, protozoa
26
protective immunity of the cytoplasm
NKs and cytotoxic T cells (96 days to be fully activated)
27
pathogens found in vesicles
plague, legionnaire's Prefer to be in vesicles to evade immune responses.
28
protective immunity of vesicles
T cell and NK dependent macrophage activation.
29
what does inflammation depend on
depends on severity (# of damaged cells)
30
what is the second line's intracellular defense mechanism
NK cells
31
what is the second line's extracellular defense mechanism
phagocytic cells
32
what is the third line's intracellular defense mechanism
CD8 cytotoxic T cells
33
what is the third line's extracellular defense mechanism
antibodies from the B cells
34
what does the third line need for both intra and extracellular defense
Both require CD4 helper T cells to be activated.
35
what does the Skin, gut, lungs, eyes/nose/oral cavity all have
tight junctions
36
what are tight junctions
proteins that seal the areas between cells.
37
what are desmosomes
like buttons with fibers that anchor cells together.
38
what are gap junctions
openings between the cells, so that cells can share whatever goes through.
39
what does fungus like in the first defense? what pathogen does it attract?
Fungus likes keratin (athletes foot).
40
what is the mechanical washing of skin and gut
longitudinal flow of air and fluid
41
what is the mechanical washing of lungs
movement of mucus by cilia. Goblet cells
42
what is the mechanical washing of eyes, nose, mouth
tears, nasal cilia.
43
what chemicals are in the skin
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.
44
what chemicals are in the gut
low pH, enzymes (pepsin), A-defensins, RegIII, cathelicidin.
45
what is in the crypt of gut cells
A-def and RegIII extremely acidic. C-type lectins (proteins that bind sugars): RegIII A-def is amphipathic protein
46
chemicals in the lungs
pulm surfactant, A-def, caths.
47
chemicals in eyes, nose, mouth
enzymes in tears and saliva (lysozyme), histatins, B-defs.
48
what do all first line components have
a microbiota Bacteria want same bacteria/environments.
49
how do NK cells kill
the directed release of lytic granules or by inducing death receptor-mediated apoptosis via the expression of Fas ligand or TRAIL.
50
what is Gram-positive’s thick cell wall is made out of
peptidoglycans (NAG and NAM)
51
how are NAG and NAM connected vertically
peptide bridges
52
what are the NAG and NAM peptide bridges called
B(1,4) glycosidic bond
53
what does lysozyme target
B (1, 4) glycosidic bonds
54
what does phospholipase A2 degrade
digests phospalipids
55
how do defensins degrade
attach to the membrane and create a pore.
56
what are the granules in granulocytes made of
filled with defensin proteins (A, B, T)
57
where are alpha defensins found
the primary granules
58
what charge are active defensins
Cationic is the active portion.
59
what are zymogens
proteins that must be cleaved in order to function.
60
what line are antimicrobial proteins found in
second line
61
where are complement proteins produced
liver
62
what are serine proteases
enzymes that cleave peptide bonds in proteins
63
what three complement proteins cause inflammation
C3a, C5a, and C5b
64
what does C3 get cleaved to
C3a and C3b
65
what is the order in which complement proteins are cleaved
C1 > C4 > C2, C3, C4-9
66
what are the four guiding principles of immuno
recognition, effector function, regulation, memory
67
what do all complement pathways converge to
C3
68
what are effector functions
the function of each immunological component an essential link between innate and adaptive immunity.
69
what are the effector functions of complement proteins
Recruit phagocytic cells to infection sites and promote inflammation. Opsonization to trigger phagocytosis (This is most important) Apoptosis
70
what is avidity in immuno
overall binding strength
70
what is special about mannose
is has specific patterns
71
what is affinity in immuno
the strength of bonding at one specific site
72
what is the lectin
any protein that binds to sugars.
73
how many lectin pathways are there
4
74
what are the four lectin paths
MBL Ficolin (M, L, H)
75
what does mbl recognize
NAG Mannose Fucose
76
characteristics of the mbl monomer
3 monomers come together to form a monomer. Trimeric clusters A total of 18 binding sites.
77
what does mbl have high avidity to
mannose and fucose residues (MASP-2 and MASP-1)
78
how is ficolin different from mbl
Different carb-binding domain.
79
what does ficolin recognize
NAG (Gram negative and positive) Teichoic acids (Gram positives)
80
what does ficolin bind to
oligosaccharides containing acetylated sugars.
81
what is the first step of lectin pathway
Activated MASP 2 (MBL or ficolin) cleaves C4 to C4a (weak trigger of inflammation) and C4b, which binds to the microbial surface.
82
second step of lectin pathway
C4b then binds C2, which is cleaved by MASP 2, to C2a and C2b, forming the C4b2a complex.
83
what is a C3 convertase
anything that has the potential to cleave C3 to C3a and b.
84
example of C3 convertase in Lectin pathway
C4b2a
85
third step of lectin pathway
C4b2a cleaves C3 to C3a and b, which binds to the microbial surface or to the convertase itself.
86
fourth step of lectin
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
where is the newly formed C3 protein bound to in step five
thioester bond
88
what is the downside of the thioester bond
Thioester is very reactive. Water can react and turn off the bond to C3.
89
step six of lectin path
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
final step of lectin pathway
Thioester bonds on C3b/C4b create covalent bonds on the surface of cells/pathogens.
91
what are the two outcomes of the lectin pathway
can result in C3b binding to the pathogen surface Or C3b is inactivated by hydrolysis (water binds to the thioester bond).
92
what proteins are in the classical pathway
C1, 2, 4 3
93
how many C1 proteins are there
C1q, r, and s
94
what classical protein is similar to MBL
C1q
95
what classical protein is similar to MASP2
C1s
96
which classical protein is a serine protease
C1s
97
what does C1s cleave to classical
C4 and C2
98
what does C4b do classical
binds to pathogen and opsonizes it Binds C2 for cleavage by C1s
99
what does C4a do classical
peptide mediator for inflammation
100
what does C2a do classical
cleaves C3 and 5
101
what does C2b do classical
precursor to vasoactive C2 kinin
102
what does C3b do classical
many molecules of c3b bind to the pathogen and act as opsonizers. unitiate amplification via alt pathway binds c5 for cleavage by c2b
103
what does c3a do classical
peptide mediator for inflammation
104
what is the function of the alternative pathway
Makes sure classical and lectin are stronger reactions
105
what are the four main components of alt pathway
C3 factors b, d, p
106
first step of alt pathway
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
second step of alt path
C3bBb (C3 convertase) cleaves many C3 to C3a and C3b.
108
third step of alt path
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
fourth step of alt path
Factor B non covalently binds to C3b on the cell surface and is cleaved into Bb.
110
what is the strongest trigger of inflammation
C5a
111
which proteins impact blood vessels to increase vascular permeability and cell-adhesion molecules.
C3a, C5a, C4a
112
why is increased permeability of vessels important
allows increased fluid leakage from vessels and extravasation of immunoglobulin and complement molecules. more migration of macros, PMN, and leukocytes
113
what cytokine triggers inflammation
TNF alpha and histamine
114
how are holes formed in the membrane for complement system
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
how is the complement system turned off
protectin (CD59)
116
How do the 3 pathways carry out effector functions
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

Immunology (11 decks)

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