6 - Immunopathogenesis 3

Question 1

When are defensins released

Answer 1

Upon binding of bacteria to TLR

Question 2

4 families of defensins

Answer 2

a-defensins
b-defensins
cathelicidins
saposins

Question 3

What releases a-defensins

What are they

Answer 3

PMNs

Azurophilic granules

Question 4

Where are b-defensins released

Answer 4

Epithelial surfaces (oral, sulcular)

Question 5

Function of defensins

Answer 5

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

Question 6

Make-up of chemokines

Answer 6

Small proteins w/ 4 cysteine residues

Question 7

What are chemokines

Answer 7

Chemotactic cytokines

Question 8

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

Answer 8

L for ligand
R for receptor

alpha
beta
gamma
delta

Question 9

What stimulates release of chemokines

Answer 9

IL-1
TNF
INF-y

Question 10

What up-regulates selectins

Answer 10

Cytokines
Complement
APPs

Question 11

What selectins are on endothelial cells

Answer 11

P-selectin

E-selectin

Question 12

What is the crossing of the cell through the epithelial membrane

Answer 12

Diapedesis

Question 13

Processing of exogenous antigens (bacteria)

Answer 13

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

Question 14

Processing of endogenous antigens (viruses)

Answer 14

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

Question 15

Does TC present to BC? Or vice versa

Answer 15

BC presents to TC

Question 16

TC co-stim molecule

BC co-stim molecule

Answer 16

CD 28 CD 154

CD 80/86 CD 40

Question 17

Role of heat shock proteins

Answer 17

Guide the synthesis, transportation, and degradation of proteins

Question 18

When is HSP on cell membranes

Answer 18

Infected cells, cell to undergo apoptosis

Question 19

Pathogenesis of microorganisms depends on ____ (4 things)

Answer 19

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

Question 20

Dysbiosis definition

Answer 20

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

Question 21

2 things for periodontitis to manifest

Answer 21

Susceptible host

Suitable environment

Question 22

AA # serotypes, most significant

Answer 22

7

B

Question 23

AA virulence factors

Answer 23

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

Question 24

PG serotypes

Answer 24

6 Kappa antigen serotypes

Question 25

PG virulence factors

Answer 25

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

Question 26

TF virulence factors

Answer 26

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

Question 27

TD virulence factors

Answer 27

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

Question 28

Initial Lesion characteristics

Answer 28

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

Question 29

Early lesion characteristics

Answer 29

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

Question 30

Established lesion characteristics

Answer 30

``` 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 ```

Question 31

Advanced lesion characteristics

Answer 31

``` 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 ```

Question 32

What does RANKL stand for

Answer 32

Receptor activator of nuclear factor kB ligand

Question 33

What expresses RANKL

Answer 33

Osteoblasts on cell membrane

Question 34

Where does RANKL binds its receptor

Answer 34

Pre-osteoclast, binds RANK

Question 35

What activates NFKb

Answer 35

Inhibitor of kappa kinase (IKK)

Question 36

What cytokines increase in periodontitis

Answer 36

IL-1 IL-6 TNF-a

Question 37

What TC increases in periodontitis

Answer 37

TH-17 | IL-17

Question 38

What BC increase

Answer 38

``` B1 cells (T independent) CD20+ BC ```