Midterm 1 Flashcards

(57 cards)

1
Q

Functional heterogeneity

A

Each cell type can express a subset of different receptor combinations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Lectins

A

Scavenger receptor, binds carbohydrates, mannoes receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Mannise receptor action

A

Surface sugar on bacterium bind to mangoes receptor extracellular domain. Macrophages invests bacteria via receptor mediated endocytosis, manise receptor travels with bacterium in endosome, but gets returned to surface before phagolysosome digests bacterium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What compliment receptor is on B cells and why

A

CR2, B cells must engulf antigen to present to helper t cell. CR2 binds iC3b and C3D.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is NF-KappaB

A

Proetein complex that controls DNA transcription and cytokine production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What do toll like receptors bind to

A

Every type of category of pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the goal of toll like receptors signaling?

A

Signaling immune cells to
1. Activate them to aquire features that increase their pathogen clearing capabilities
2. Induce secretion if cytokines that activate cytokines and adaptive immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

LRR

A

Leucine rich repeat region, pathogen recognition domain on TLRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Recognition factor for TLR4

A

Lipopolysaccharide, released from bacterial cell surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

LBP

A

Lipopolysachharide binding protein binds LPS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

TLR4 to TLR4 complex pathway

A
  1. Macrophage engulfed bacterium and releases LPS bound by LPB.
  2. Endosome delivers LPS to CD14 exocytic vesicles
  3. LPS is transferred to CD14 (coreceptor) on plasma membrane.
  4. TLR4, LPS, and MD2 (coreceptor) forms a complex on plasma membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

TLR4 complex to kinase cascade

A

1.MyD88 (adaptor protein) binds to TIR domain of TLR4
2. IRAK4 binds to MyD88 and is activated
3. IRAK4 phosphorylation itself and dissociate from MyD88 then phosphosphorylates TRAF6 (adaptor protein)
4. TRAF6 initiates a kinase cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Kinase cascade to activation of NF-kappaB

A
  1. Kinase cascade activates IKK ( I kappa beta kinase) by phosphorylation
  2. IKK phosphorylation inhibitory subunits of Ikappabeta/NF-kappaB complex
  3. NF-kappaB transcription factor is free to be transcribed.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

IL-1Beta function

A

Causes secretion of inflammatory cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

TNF-a

A

Induces more permeable blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

IL-6

A

Induces fat and muscle to metabolize and generate heat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

CXCL8

A

Recruits neutrophils to infected tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

CCL2

A

Recruites monocytes to infected tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

IL-12

A

Recruits and activates natural killer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Cytokine def’n

A

Small soluble molecule that can bind to something in the immune system. Short lived, act on short distances.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Interferons

A

Cytokines released during a viral infection

24
Q

Why are type 1 interferon generated quickly

A

All human cells can generate type 1 interferons. Receptors are located on all nucleated cells all the time.

25
Virus to IRF3 and IRF7 transcription factor.
1. Viral RNA binds to RIG1 2. RIG1 bound to RNA now binds to MAVS 3. Complex initiates signal via TRAF6 4. TRAF6 activates IRF3 and IRF7
26
What response does IRF3 generate
IFN-BETA response. IFN-Beta binds type 1 IFN receptors on adjacent cells, practice response
27
What response does IRF7 Induce
Autocorrect IFN-alpha response
28
Plasmacytoid dendritic cells
Job is to produce IFNs. Use toll like receptors to detect infection.
29
What to INF Alpha and Beta do
Induces synthesis of cellular proteins that will inhibitory viral replication in a cell.
30
Caspase 1
Protease that cleaves inactive IL-1Beta into active form
31
Macrophage adaptation for quick immune response
Activated IL-1beta is exits through a pore made by gasdermin D and the macrophage dies. Small portion of macrophages.
32
What does IL-1Beta release trigger in other macrophages?
Synthesis and release of 5 cytokine categories.
33
Overview of neutrophils recruitment, Rolling adhesion
Rolling adhesion: Recruitment of neutrophils from blood to tissue is mediated by complimentary pairs of adhesion molecules.
34
Selectins
Adhesion molecules on neutrophils and endothelial cells that bind glyvoproteins
35
S-Le*
Small Lewis carbohydrates. Get bound by selectins to slow neutrophils as they flow through blood
36
Rolling adhesion to tight binding (neutraphils)
Many weak interactions with iCAM-1 (endothelial cells) and LFA-1 on neutrophils
37
Rolling adhesion
38
CXCL8 role in neutrophils transport
CXCL8 binds to gpcr, g protein activates and and disociates into 2 subunits and chemicals takes neutrophils to the site of infection.
39
What do neutrophils do
They have toxic granules that destroy bacteria once engophed after being recognized by a receptor. Short lived.
40
NETosis
Nucleus of neutrophils swells then bursts and extrudes chromatin to capture microbes
41
42
Pyrogen
Cytokines and other molecules that produce fever which negatively impacts most pathogens
43
Synthesis of Acute phase proteins
Released in response to bacteria inducing macrophages to produce IL6 which acts on hepatocytes to induce synthesis of acute phase proteins
44
CRP
Pentraxin that binds a variety if pathogens and acts as an sopsonjn triggering the classical pathway of compliment. High in acute infection
45
Serum amyloid A protein
Stimulates production of cytokines by binding to cell surface receptors on macrophages.
46
MBL
Mannose binding lectin. Acute phase proteins that binds to mangoes on pathogens, not om human cells.virvulates serum with HDL.
47
MASP1 AND MASP2
MBL associates serine protease that cleave compliment. MBL binds to pathogen then cleavage occurs.
48
MBL lectin pathway of compliment activation
MASP2 cleaves C4 into C4a and C4b, C4b attaches ro microbe. MASP2 then leaves C2 into C2a and b and c2b attaches to C4b and forms C4bC2a
49
C4bC2a
C3 convertase. Binds C3 and cleaves into C3a and b C3b attaches to surface.
50
Classical pathway of compliment activation overview
CRP can activate as well as igG and igM. CRP bound to phosphorylcholine (pathogen) binds C1. C1 acts like MBL to create C3 convertases.
51
52
C1 classical pathway
C4b binds to pathogen surface, C1 cleaves C2 into a and b subunits and C2a binds to C4b forming C4bC2a (C3 convertase)
53
Natural killer cells
Need to know target is for sure foreign. Discharge toxic granules.
54
Type 1 interferons and NK cells
INF BETA AND ALPHA reach NK cell. Induce apoptosis.
55
IL12 and Nk cells.
Recruits eachother. Macrophages release cytokines that revruit NK cells. Macrophage and NK cells conjugate and macrophage delivers IL12. NK cells is now activated and proliferate into effector NK cells.
56
Effector NK cells
Secrete IFN-Y which binds to receptor in macrophage and increases phagocytosis and cytokine secretion.
57
Dendritic cells and NK cells
When NK cells are abundant, they outbumber dendritic cells and kill them. When they are scarce dendritic cells mature and initiate the adaptive immune response.