Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Perio Lecture Series > 6 - Immunopathogenesis 3 > Flashcards

6 - Immunopathogenesis 3 Flashcards

1
Q

When are defensins released

A

Upon binding of bacteria to TLR

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

4 families of defensins

A

a-defensins
b-defensins
cathelicidins
saposins

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

What releases a-defensins

What are they

A

PMNs

Azurophilic granules

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

Where are b-defensins released

A

Epithelial surfaces (oral, sulcular)

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

Function of defensins

A

Signaling molecules that modulate the inflammatory response, chemokine production, wound healing, etc

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

Make-up of chemokines

A

Small proteins w/ 4 cysteine residues

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

What are chemokines

A

Chemotactic cytokines

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

4 groups made up of 2 distinct populations. What are they?

A

L for ligand
R for receptor

alpha
beta
gamma
delta

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

What stimulates release of chemokines

A

IL-1
TNF
INF-y

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

What up-regulates selectins

A

Cytokines
Complement
APPs

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

What selectins are on endothelial cells

A

P-selectin

E-selectin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the crossing of the cell through the epithelial membrane

A

Diapedesis

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

Processing of exogenous antigens (bacteria)

A

1) Ag phagocytized (endocytosis)
2) Endosome fuses w/ lysosome
3) Ag broken up
4) MHC II + invariant molecule assembled in ER and transported by Golgi to lysosome
5) Ag replaces invariant molecule, transported to PM for CD4+ TC

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

Processing of endogenous antigens (viruses)

A

1) Viral proteins in cytosol degraded in proteasomes
2) Transporter associated with antigen processing (TAP) picks up antigen and assembled in MHC I in ER
3) Transported in Golgi to cell membrane for CD8+ TC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Does TC present to BC? Or vice versa

A

BC presents to TC

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

TC co-stim molecule

BC co-stim molecule

A

CD 28 CD 154

CD 80/86 CD 40

17
Q

Role of heat shock proteins

A

Guide the synthesis, transportation, and degradation of proteins

18
Q

When is HSP on cell membranes

A

Infected cells, cell to undergo apoptosis

19
Q

Pathogenesis of microorganisms depends on ____ (4 things)

A

1) Colonize and form biofilm
2) Invade host tissue
3) Virulence factors
4) Activate destructive immune response

20
Q

Dysbiosis definition

A

Pathologic shifts in microbiota occur by overgrowth of organisms normally present in lower numbers

21
Q

2 things for periodontitis to manifest

A

Susceptible host

Suitable environment

22
Q

AA # serotypes, most significant

A

7

B

23
Q

AA virulence factors

A

Leukotoxin –> pore-forming protein that in low dose leads to apoptosis, high dose to necrosis
GroEL –> chaperone protein
FImbriae
Inhibit TC cytokine production

24
Q

PG serotypes

A

6 Kappa antigen serotypes

25
Q

PG virulence factors

A

Leukotoxin –> pore-forming protein that in low dose leads to apoptosis, high dose to necrosis
Gingipains –> proteolytic Arg-X and Lys-X that degrades AB and complement
GroEl
Fimbriae

26
Q

TF virulence factors

A

Cell surface proteases for attachment to fibroblasts/PMNs
GroEL
Major surface antigen –> produce proinflammatory cytokines
Invade epithelial cells

27
Q

TD virulence factors

A 
Membrane sheath (like lipoteichoic acid)
Major sheath protein
Flagellum
Dentilisin and trepolisin proteases
Invades CT
28
Q

Initial Lesion characteristics

A 
Appears 2-4 days
Vasculitis
Loss of perivascular collagen
PMNs
Increased GCF
Alteration of coronal JE
29
Q

Early lesion characteristics

A 
Appears 4-7 days
Vasculitis
Loss perivascular collagen 60-70%
Leukocytes subjacent to JE (TH1)
GCF increases
Basal JE proliferates laterally
Fibroblast alterations
30
Q

Established lesion characteristics

A 
Appears 2-3 weeks
Lesion at bottom of sulcus
Plasma cells predominate
Extravascular ABs
CT loss, fibrosis
JE proliferation and apical and lateral extension
No bone loss
Sharpey's fibers break down
31
Q

Advanced lesion characteristics

A 
Plasma cells predominate
Pocket formation
Lesions extends subjacent to pocket
CT loss
Extension of lesion into bone and PDL
Conversion of bone marrow distant from lesion to CT
32
Q

What does RANKL stand for

A

Receptor activator of nuclear factor kB ligand

33
Q

What expresses RANKL

A

Osteoblasts on cell membrane

34
Q

Where does RANKL binds its receptor

A

Pre-osteoclast, binds RANK

35
Q

What activates NFKb

A

Inhibitor of kappa kinase (IKK)

36
Q

What cytokines increase in periodontitis

A

IL-1
IL-6
TNF-a

37
Q

What TC increases in periodontitis

A

TH-17

IL-17

38
Q

What BC increase

A 
B1 cells (T independent)
CD20+ BC

Perio Lecture Series (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions