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Host and Defense PMO > German Induced immunity > Flashcards

German Induced immunity Flashcards

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1
Q 
What are the resident macrophages in the
Brain
bone
liver
skin
A

Brain: microglia
Bone: osteoclasts
Liver: Kupffer cells
Skin: Langerhans cells

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2
Q

What do diacyl lipopeptides recognize?

A

TLR-2 and TLR-6

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3
Q

What do triacyl lipopeptides recognize?

A

TLR-2 and TLR-1

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4
Q

What does flagellin recognize?

A

TLR-5

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5
Q

What does LPS recognize?

A

TLR-4 and MD-2

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6
Q

What does dsRNA bind?

A

TLR-3

In the endosome

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7
Q

What does ssRNA bind?

A

TLR-7

In the endosome

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8
Q

What does CpG DNA bind?

A

TLR-9

In the endosome

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9
Q

Which cells are responsible for controlling the immune responses to parasites

A

Basophils

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10
Q

What are some macrophage receptors?

A

Mannose receptor CD206
Complement receptors 3 and 4 (Mac1, CD11b/CD18)
Dectin-1
Macrophage receptor with collagenous structure (MARCO)
Scavenger receptor A (SR-A)
SR-B (CD36)
LPS receptor (CD14)

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11
Q

What is the pathway for LPS Cytokine production?

A

TLR4, MD2, CD14 and LPS form at the macrophage surface. MyD88 binds TLR4 and activates IRAK4 to phosphorylate TRAF6, which leads to a cascade that phosphorylates IKK. IKK phosphorylates IkB, leading to its degradation and releasing NFkB, which enters the nucleus, transcribes inflammatory cytokines which are released all around.

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12
Q

What is NOD and what does it do?

A

Nucleotide-binding Oligomerization Domain. Recognizes bits of chopped up bacteria in macrophage cytoplasm, dimerizes, and phosphorylates TAK1 to phosphorylate IKK and then make cytokines

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13
Q

How do Inflammasomes work?

A

IL-1B binds to receptors for it, MyD88 pathway is turned on and pro- IL1B is turned on. Caspase 1 cleaves it and IL-1B is released.

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14
Q

How does Caspase get turned on?

A

NLRP3 oligermizes and cleaves procaspase1 into caspase 1 (this is a checkpoint that prevents an inflammatory response if it it turned off)

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15
Q

What are the 6 families of cytokines?

A 
Class I
Class II
IL1
IL17
TNF
Chemokines
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16
Q

Cytokines use what kind of signaling?

A

JAK-STAT

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17
Q

What 5 inflammatory cytokines to macrophages release?

A 
IL-1B 
TNF-a
IL-6
CXCL8
IL-12
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18
Q

What does IL1B do?

A 
Activates endothelium, 
activates lymphocytes
destroys tissue
Increases access of effector cells
Fever
Production of IL6
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19
Q

What does TNFa do?

A

increases endothelial permeability, allows increased entry of IgG and complement and cells and increased drainage to lymph nodes. Fever, Mobilization of metabolites, shock

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20
Q

What does IL6 do?

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A

Activates lymphocytes, increases antibody production, fever, induces acute-phase protein production

21
Q

What does CXCL8 do?

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A

Chemotaxis, recruits neutrophils, basophils, and Tcells

22
Q

What does IL12 do?

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A

Activates NK cells, induces differentiation of CD4 T cells in to Th1 cells.

23
Q

What are acute phase proteins?

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A

C-reactive protein, mannose-binding lectin. Found in liver, activate complement. IL-6 turns on liver production

24
Q

How is adaptive immune response turned on?

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A

TNFa stimulates migration to lymph nodes and maturation

25
What does C-reactive protein do other than complement?
Binds to phosphocholine on bacterial surfaces, acting as an opsonin
26
What causes septic shock syndrome?
Systemic infection with gram-negative bacteria. Macrophages make TNFa, which lets lymph and cells leak out everywhere. Vessels collapse, coagulation, wasting, organ failure, death.
27
What are the four kinds of chemokine?
CL, CCL, CXCL, CX3CL
28
What do adhesion molecules do?
Tether leukocytes
29
What do proteases do?
Open basement membranes (MMPs and Elastase)
30
What are the 4 steps of diapedesis?
``` Rolling (selectin-mediated adhesion) Rolling adhesion (CXCL8 Receptor binds.) Tight binding (LFA-1 and ICAM-1) Diapedesis Migration ```
31
What is the primary innate killer?
Neutrophils
32
What are the four neutrophil granule types?
``` Azurophil granules (myeloperoxidase, defense's, Cathepsin G) Specific granules (lactoferrin, collagenase, lysozyme) Gelatins granules (gelatinase, lysozyme) Secretory granules (CR1, CR3, CD14, CD16) ```
33
What are the three steps in Oxidative burst?
1. Make a superoxide using NADPH 2. Dismutase the superoxide to make H2O2 3. Catalase to make water and oxygen out of H2O2
34
What are the 3 kinds of Neutrophil extracellular traps?
1. Non-lytic, DNA 2. Non-lytic, mitochondrial DNA 3. Lytic
35
What cells initiate adaptive immunity?
Dendritic cells
36
What are dendritic cells derived from?
Monocytes
37
What causes the interferon response?
Viral infections
38
What causes synthesis of Interferons?
IRF3 in cells, made by TRAF6
39
What are two things that bind viral RNA to make interferons?
RLR-retinoic acid inducible gene-I like receptor | MAV- mitochondrial antiviral signaling protein
40
Type I vs Type II interferons
INFa and INFB= Type I | IFNg=Type II
41
What releases interferons?
Diseased or stressed cells, leukocytes
42
What activates NK cells?
Interferons. Proliferation, differentiation into cytotoxic effector cells. Then effector NK cells induce apoptosis in virally infected cells
43
What regulates the transition from innate to adaptive immune response?
NK cells
44
What keeps NK cells from killing healthy cells?
MHC I receptors
45
How does a macrophage turn on a NK cell?
IL12 and IL15
46
When turned on by kissing a macrophage, what does a NK cell make?
IFN-g, which turns on the macrophage to increase phagocytosis and secrete inflammatory cytokines
47
What happens when there are mor NK cells than dendritic? Vis versa?
When too many NK cells, they kill dendritic cells. When few NK cells, they drive dendritic cells to mature and start adaptive immunity
48
What are the inflammatory cytokines?
``` IL-1B TNF-a IL-6 CXCL-8 IL-12 ```

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