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Host and Defense PMO > German Induced immunity > Flashcards

German Induced immunity Flashcards

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?

A

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

21
Q

What does CXCL8 do?

A

Chemotaxis, recruits neutrophils, basophils, and Tcells

22
Q

What does IL12 do?

A

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

23
Q

What are acute phase proteins?

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?

A

TNFa stimulates migration to lymph nodes and maturation

25
Q

What does C-reactive protein do other than complement?

A

Binds to phosphocholine on bacterial surfaces, acting as an opsonin

26
Q

What causes septic shock syndrome?

A

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
Q

What are the four kinds of chemokine?

A

CL, CCL, CXCL, CX3CL

28
Q

What do adhesion molecules do?

A

Tether leukocytes

29
Q

What do proteases do?

A

Open basement membranes (MMPs and Elastase)

30
Q

What are the 4 steps of diapedesis?

A 
Rolling (selectin-mediated adhesion)
Rolling adhesion (CXCL8 Receptor binds.) 
Tight binding (LFA-1 and ICAM-1)
Diapedesis
Migration
31
Q

What is the primary innate killer?

A

Neutrophils

32
Q

What are the four neutrophil granule types?

A 
Azurophil granules (myeloperoxidase, defense's, Cathepsin G)
Specific granules (lactoferrin, collagenase,  lysozyme)
Gelatins granules (gelatinase, lysozyme)
Secretory granules (CR1, CR3, CD14, CD16)
33
Q

What are the three steps in Oxidative burst?

A
  1. Make a superoxide using NADPH
  2. Dismutase the superoxide to make H2O2
  3. Catalase to make water and oxygen out of H2O2
34
Q

What are the 3 kinds of Neutrophil extracellular traps?

A
  1. Non-lytic, DNA
  2. Non-lytic, mitochondrial DNA
  3. Lytic
35
Q

What cells initiate adaptive immunity?

A

Dendritic cells

36
Q

What are dendritic cells derived from?

A

Monocytes

37
Q

What causes the interferon response?

A

Viral infections

38
Q

What causes synthesis of Interferons?

A

IRF3 in cells, made by TRAF6

39
Q

What are two things that bind viral RNA to make interferons?

A

RLR-retinoic acid inducible gene-I like receptor

MAV- mitochondrial antiviral signaling protein

40
Q

Type I vs Type II interferons

A

INFa and INFB= Type I

IFNg=Type II

41
Q

What releases interferons?

A

Diseased or stressed cells, leukocytes

42
Q

What activates NK cells?

A

Interferons. Proliferation, differentiation into cytotoxic effector cells. Then effector NK cells induce apoptosis in virally infected cells

43
Q

What regulates the transition from innate to adaptive immune response?

A

NK cells

44
Q

What keeps NK cells from killing healthy cells?

A

MHC I receptors

45
Q

How does a macrophage turn on a NK cell?

A

IL12 and IL15

46
Q

When turned on by kissing a macrophage, what does a NK cell make?

A

IFN-g, which turns on the macrophage to increase phagocytosis and secrete inflammatory cytokines

47
Q

What happens when there are mor NK cells than dendritic? Vis versa?

A

When too many NK cells, they kill dendritic cells. When few NK cells, they drive dendritic cells to mature and start adaptive immunity

48
Q

What are the inflammatory cytokines?

A 
IL-1B
TNF-a
IL-6
CXCL-8
IL-12

Host and Defense PMO (8 decks)

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