Immune Defense Flashcards

1
Q

What are the 5 physical barriers and entry portals?

A
  • skin
  • respiratory tract
  • GI tract
  • urogenital tract
  • blood & lymphatic systems
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2
Q

How is the skin protected?

A
  • ketatinized surface
  • tight epithelial junctions
  • low pH (lactic and fatty acids)
  • endogenous flora
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3
Q

How is the respiratory tract protected?

A
  • branching airways
  • mucus
  • mucocilliary movement
  • coughing
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4
Q

How is the GI tract protected?

A
  • low pH
  • cilia
  • endogenous flora
  • diarrhea & vomiting
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5
Q

How is the urogenital tract protected?

A
  • flow sheer forces
  • low pH (vagina)
  • endogenous flora)
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6
Q

How is the blood and lympthatic system protected?

A

clotting

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7
Q

What are the 3 innate soluble factors?

A
  • antimicrobial peptides
  • complement
  • surfactant proteins
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8
Q

What are the 2 adaptive soluble factors?

A
  • antibodies
  • cytokines
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9
Q

What are the 2 innate cellular factors?

A
  • phagocytic cells
  • NK cells
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10
Q

What are the 3 adaptive cellular factors?

A
  • B cells
  • T cells
  • memory (immunity)
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11
Q

What makes AMPs?

A

epithelial cells and leukocytes

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12
Q

What do AMPs do?

A
  • defensins
  • use their amphipathicity to create pores in the cell membrane
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13
Q

How do AMPs not attack self?

A
  • We have sterols in our cell membrane which are nonpolar
  • weak van der waal’s forces
  • bacteria don’t and thus have more - charges for the + charged AMPs to bind to
  • strong ionic bonding
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14
Q

What does C3 do?

A

Tells complement system where to form MAC

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15
Q

What does C3a do?

A

chemoattractant for immune cells

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16
Q

How does C3b amplification work?

A

C3b binds to Factor B to make C3 convertase which creates more C3b

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17
Q

How does C3b amplification stop?

A
  • once the microbe is gone there is no surface for C3 to attach to and to be cleaved into C3b
  • no C3b created to bind to Factor B and create C3 convertase
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18
Q

How does the classical pathway relate to C3 convertase?

A

Multiple antibody bindings lead to the creation of C3 convertase

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19
Q

What binds the constant region of an antibody?

A

Ig receptors (FcgammaR)

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20
Q

What’s great about IgG?

A
  • it’s a great opsonin which activates the complement system and promotes phagocytosis
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21
Q

What’s great about IgA?

A

good at neutralizing antigens (pathogenic toxins and adhesins)

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22
Q

What’s great about IgM?

A

Great complement activator

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23
Q

What happens when antibodies and complement are both activated?

A
  • double receptor activation = more chance of phagocytosis
  • MAC simultaneously lyses pathogen
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24
Q

How does the Lectin pathway work?

A

Lectin binds sugar PAMPs to create C3 convertase

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25
How does the Alternative Activation Pathway work?
* C3 tickover (spontaneous cleavage) binds Factor B to form C3 convertase
26
How does the Alternative Activation Pathway not hurt us?
* negative factors cleave C3b into iC3b to prevent complement activation * Ex - Factor H (sialic acid) is mostly unique to mammalian cells
27
How are the alveoli protected?
* surfactant fluid helps prevent alveolar sticking and contains surfactant proteins * macrophages wander around in the surfactant fluid
28
What produces surfactant proteins?
airway epithelial cells (Clara cells) and alveolar type II cells
29
What are the components of surfactant proteins?
* N-terminal non-collagenous domain * collagenous region * alpha helical coiled coil * Carb recoginition domain (CRD) head - lectin domain
30
Head or tail model
* if the surfactant protein (SP) head binds to SIRPalpha = all clear * if *multiple* SP tails bind = head bound to pathogen = CD91/calreticulin activation = phagocyte activation and phagocytosis
31
What 3 things do surfactant proteins do?
* Head or tail model * clump pathogens to be coughed up * directly kill pathogen
32
What are the 3 antigen presenting cells
* macrophages * dendritic cells * B cells
33
How does phagocytosis kill a pathogen?
* acidification of phago(lyso)some * lysosomal enzymes * ROS vis phox complex and NADPH-oxidase * RNS
34
What do neutrophil's granules do?
* kill microbe - ex- myeloperoxidase makes bleach (HOCl) * inhibit microbe growth - ex - lactoferrin sequesters iron
35
MR recognises what?
mannose
36
TLR4 recognizes what?
mannan
37
TLR2 recognizes what?
phosphomannan
38
What do TLR2 and TLR4 require?
MyD88 as a signal protein
39
Dectin-1 recognizes what?
beta-glucan
40
SR and CR recognize what?
glucans possibly
41
IL-10
supresses T cell proinflammatory cytokine production
42
IL-23
promotes Th0 to Th17
43
IL-12
promotes Th0 to Th1
44
IFNgamma
produced by Th1 cells to activate macrophages
45
TNFalpha
local inflammation
46
What bridges innate and adaptive immunity?
antigen presentation
47
What is required for antigen presentation?
* APC finds naive T cell * MHC+antigen-TCR * B7-CD28 costimulatory
48
Steps to activate a macrophage
* APC migrates to lymph tissue * meets naive T cell * MHC+antigen-TCR * B7-CD28 co stimulatory * this leads to activated T cell * activated Th1 cell migrates out of lymph tissue and meets macrophage * MHC+antigen-TCR * CD40-CD40L * Th1 releases IFNgamma and TNFalpha
49
How do you create a Th1?
Th0 + IL12 + IFNalpha
50
How do you create Th2?
Th0 + IL4
51
How do you create Th17?
Th0 + IL6 + TGFbeta + IL23
52
What does macrophage activation do?
* UP B7 and CD40 costimulatory molecules * UP ROS and NOS production * UP TNFalpha and IFNgamma receptor expression * UP phagolysosomal fusion * UP MHC display
53
What do Th17 cells so?
* mucosal immunity * secrete IL17 and IL22 which causes release of AMPs, chemokines, and PMN growth factors
54
What do Th1 cells do?
cell mediated immunity by activating macrophages
55
What do Th2 cells do?
Activate B cells which leads to antibody production
56
How do B cells make antibodies?
* naive B cell BCR-antigen * finds activated Th2 * MHC+antigen-TCR * CD40-CD40L * activated Th2 cell produces IL4 and IL6 which create a mature B cell * B cell divides into plasma and memory cells * plasma cells produce antibodies
57
Nonpathogenic microbe
58
Opportunistic microbe
59
Primary pathogen
60
Chronic/latent infection
60
Chronic/latent infection