Immunology: Theme 2: Immunity To Micro Organism

Front 1

What is a pathogen?

Back 1

Any organism with the potential to cause disease

Hint 1

including oppurtunistic pathogens

Front 2

Name the 4 kinds of pathogens?

Back 2

bacteria, virus, funghi and parasites?

Front 3

How can pathogens cause damage?

Back 3

Exotoxin release, Endotoxin release & Direct cytopathic effect.

Hint 3

Exotoxin: vibrio cholerae
Endotoxin: Yersinia Pestis
Direct cytopathic: influenza virus

Front 4

Extracellular: Interstitium, blood and lymph.

What is the innate defense mechanism?

Back 4

complement, macrophages and neutro's

Hint 4

organism: viruses, bacteria, protozoa, funghi, worms.

Front 5

What is the innate defense on epithelial surfaces

Back 5

antimicrobial peptides

Hint 5

neisseria gonorrhoeae
candida albicans

Front 6

What is the innate defense against intracellular cytoplasmic infection?

Back 6

NK cells

Hint 6

organism: viruses, listeria and protozoa

Front 7

What is the innate defense against intracellular vesicular infection?

Back 7

Activated macrophages

Hint 7

Organisms: mycobacteria, trypanosomes, Cryptococcus neoformans.

Front 8

Innate defense consist of two parts. Name the two parts?

Back 8

Recognition and Effector Cells

Front 9

Innate defense, two parts

What are the recognition mechanisms?

Back 9

Complement and Macrophages

Front 10

What are complement

Back 10

plasma proteins, especially proteolytic enzymes or proteases

Hint 10

made by liver, circulate in inactive forms as zymogens. infection triggers complement activation.

Front 11

C3 cascade

Back 11

draw it

Front 12

What are the three pathways of complement activation

Back 12

Alternative, Lectin and Classical pathway.

Front 13

function of c3b binding on pathogen surface

Back 13

opsonization, chemotaxis of inflammatory cells and lysis

Front 14

Why do we need complement control proteins?

Back 14

If not, then due to progressive amplification of C3 cleavage on pathogen surface, depletion of C3

Front 15

Two kinds of complement control proteins

Back 15

soluble: interacts with c3b on human and microbial surfaces

fixed on membrane proteins: prevention complement fixation at the cell surface.

Front 16

Soluble complement control proteins,

stimulating?

Back 16

Properdin (factor P)

Hint 16

stabilizes C3Bb on pathogen surface.

Front 17

Soluble complement control proteins,

inhibiting?

Back 17

Factor H and Factor I

Hint 17

Factor H binds on C3b and recruits factor I to cleave C3b into iC3b.

Front 18

Membrane Complement control proteins,

Inhibiting

Back 18

DAF (decay-accelerating factor)
&
MCP (Membrane co-factor protein)

Hint 18

DAF touches C3bBb and C3b seperates from Bb part.

MCP: seperation, but also factor I recruiment. cleavage to iC3b

Front 19

strategy Streptococcus pyogenes and stayphylococcus aureus

Back 19

sialic acid expression, mimic human cell, recruits factor H and degrades the bounded C3b.

Front 20

function complement control proteins

Back 20

discrimination of non-self from self.

protection for depletion

Front 21

first innate effector cell?

Back 21

macrophage

Hint 21

in liver: kupffer cells

Front 22

how does macrophage recognize the C3b on pathogen surface?

Back 22

CR1 complement receptor 1

Hint 22

coating by c3b is calles opsonization.

Front 23

function CR1

Back 23

recognition C3b and enhancement macrophage for phagolysosome.

protects against C3b coating on self-cells like DAF and MCP.

Front 24

function CR 3 and 4 (on macrophage.)

Back 24

recogntion of iC3b and LPS.

Front 25

terminal complement components (lysis)

Back 25

C5-C9

Front 26

Forming membrane attack complex

Back 26

C3b2Bb + C5-C9

Front 27

function c5a and c3a

Back 27

chemotaxis with c5a > c3a

Hint 27

cave:
as anaphylatoxins, possible anaphylactic shock.

Front 28

alternative c5 convertase

Back 28

c3b2Bb

Front 29

protection and regulation of terminal complement components

Back 29

soluble: s protein, clusterin, factor J

Membrane: HRF and CD59 and DAF

Hint 29

if deficiency in lipid tail of HRF, CD59, DAF, then paroxysmal nocturnal hemoglobinuria.

Front 30

function anaphylatoxins c5a and c3a

Back 30

degranulation mast cells, histamines & TNF-alfa.

increase permeability

inflammation ;)

Hint 30

migration monocytes and neutrophils, more plasma proteins as complement.

Front 31

plasma proteins that limit the spread of infection

Back 31

coagulation system, kinin system (vasodilation), protease inhibitors as alfa2-macroglobulins.

Front 32

type receptors on macrophage

Back 32

phagocytic receptors (mannose, CR3, glucan, scavenger receptor)
and
receptors promote cytokines secretion. (Toll-Like receptors)

Front 33

TLR endosomes?

Back 33

TLR 3, 7, 8, 9.

Front 34

TLR1:TLR2 heterodimer

ligands & cells

Back 34

lipopeptides

monocytes, dc, eo's baso's mast cells

Hint 34

bacteria.

Front 35

TLR2:TLR6 heterodimer

ligands and cells

Back 35

lipoteicoic acid

mono's dc' eo's baso' mast cells

Hint 35

gram positive bacteria.

Front 36

TLR 3

ligands and cells

Back 36

Double stranded viral RNA

NK cells

Front 37

TLR 4

ligands and cells

Back 37

LPS

Macrophages, DC, Eo's and mast cells

Hint 37

Gram negative bacteria

Front 38

TLR 5

Back 38

Flagellin

Intestinal epithelium

Hint 38

motile bacteria with flagellum

Front 39

TLR 7

Back 39

ssvirRNA

DC, NK, EO's, B cells

Hint 39

HIV

Front 40

TLR8

Back 40

ssvirRNA

NK cells

Hint 40

Influenza

Front 41

TLR 9

Back 41

unmethylated CpG-rich DNA

dc, b cells, eo's baso/s

Hint 41

bacteria and viruses

Front 42

Co-receptors TLR4

Back 42

MD2, CD14

and ligand LPS.

Front 43

two different cytokine response

Back 43

Type 1 interferons: IFN-alfa/beta
&
Inflammatory cytokines

Hint 43

TLR4 is the only one that could use both

Front 44

Co-receptors TLR4

Back 44

MD2, CD14

and ligand LPS.

Front 45

Inflammatory cytokines pathway

Back 45

TLR4, MyD88, IRAK4, NFkB,

Front 46

two different cytokine response

Back 46

Type 1 interferons: IFN-alfa/beta
&
Inflammatory cytokines

Hint 46

TLR4 is the only one that could use both

Front 47

Type 1 interferons pathway

Back 47

TLR 4 or 3, IRF 3, IFNalfa/beta

Front 48

Macrophage secretion inflammatory cytokines due to TLR4

Back 48

IL-1, IL-6, IL8/CXCL8, IL-12 and TNF-alfa

Front 49

Inflammatory cytokines pathway

Back 49

TLR4, MyD88, IRAK4, NFkB,

Front 50

inflammatory cytokines

function CXCL8

Back 50

chemokines, attraction via concentration gradient

recruitment neutrophils via CXCR1 and CXCR2

Front 51

Type 1 interferons pathway

Back 51

TLR 4 or 3, IRF 3, IFNalfa/beta

Front 52

binding CXCL8 on CXCR1/2 on neutrophils, two effects?

Back 52

it can leave blood and enter tissue

guidance through concentration gradient.

Front 53

Macrophage secretion inflammatory cytokines due to TLR4

Back 53

IL-1, IL-6, IL8/CXCL8, IL-12 and TNF-alfa

Front 54

inflammatory cytokines

function IL-12

Back 54

activation NK lymphocytes

Front 55

inflammatory cytokines

function CXCL8

Back 55

chemokines, attraction via concentration gradient

recruitment neutrophils via CXCR1 and CXCR2

Front 56

inflammatory cytokines

function IL-1, TNF-alfa

Back 56

IL-1: activates vascular endothelium, activates lymphocytes, local tissue destruction, production of IL-6 and fever

TNF-alfa: activates vascular endothelium, vascular permeability, increased entry and increase fluid drainage to lymph nodes and fever

cave: shock.

Front 57

binding CXCL8 on CXCR1/2 on neutrophils, two effects?

Back 57

it can leave blood and enter tissue

guidance through concentration gradient.

Front 58

Co-receptors TLR4

Back 58

MD2, CD14

and ligand LPS.

Front 59

Inflammatory cytokines

function IL-6

Back 59

fever, induces acute-phase proteind production by hepatocytes.

Front 60

inflammatory cytokines

function IL-12

Back 60

activation NK lymphocytes

Front 61

inflammatory cytokines

function IL-1, TNF-alfa

Back 61

IL-1: activates vascular endothelium, activates lymphocytes, local tissue destruction, production of IL-6 and fever

TNF-alfa: activates vascular endothelium, vascular permeability, increased entry and increase fluid drainage to lymph nodes and fever

cave: shock.

Front 62

two different cytokine response

Back 62

Type 1 interferons: IFN-alfa/beta
&
Inflammatory cytokines

Hint 62

TLR4 is the only one that could use both

Front 63

Inflammatory cytokines pathway

Back 63

TLR4, MyD88, IRAK4, NFkB,

Front 64

Inflammatory cytokines

function IL-6

Back 64

fever, induces acute-phase proteind production by hepatocytes.

Front 65

Type 1 interferons pathway

Back 65

TLR 4 or 3, IRF 3, IFNalfa/beta

Front 66

Macrophage secretion inflammatory cytokines due to TLR4

Back 66

IL-1, IL-6, IL8/CXCL8, IL-12 and TNF-alfa

Front 67

inflammatory cytokines

function CXCL8

Back 67

chemokines, attraction via concentration gradient

recruitment neutrophils via CXCR1 and CXCR2

Front 68

binding CXCL8 on CXCR1/2 on neutrophils, two effects?

Back 68

it can leave blood and enter tissue

guidance through concentration gradient.

Front 69

inflammatory cytokines

function IL-12

Back 69

activation NK lymphocytes

Front 70

inflammatory cytokines

function IL-1, TNF-alfa

Back 70

IL-1: activates vascular endothelium, activates lymphocytes, local tissue destruction, production of IL-6 and fever

TNF-alfa: activates vascular endothelium, vascular permeability, increased entry and increase fluid drainage to lymph nodes and fever

cave: shock.

Front 71

Inflammatory cytokines

function IL-6

Back 71

fever, induces acute-phase proteind production by hepatocytes.

Front 72

function acute-phase response induced by il-1, il-6 and tnf-alfa.

Back 72

enhance fixation of complement at pathogen surfaces via mannose-binding lectin and CRP.

Front 73

CRP binding to

Back 73

phosphocholine of LPS, not of human cell membranes.

Front 74

function crp

Back 74

opsonization and classical pathway.

Front 75

classical pathway c3 convertase

Back 75

C2aC4b. and at CRP c1 is needed.

Front 76

reaction of cell when infected by virus

Back 76

production of type 1 interferons
ifnalfa/beta

Front 77

Function IFN-alfa and IFN-beta

Back 77

signaling autocrine and paracrine to induce interferon response

Front 78

what is interferon repsonse

Back 78

1.degradation of intracellular viral RNA
2. inhibition protein synthesis.
3. increase expression of ligands for receptors on NK cells
MIC-A and MIC-B --> NK cells' NKG2D
4. activate NK cells to kill virus-infected cells.

Hint 78

IFNalfa/beta increase base level cytotoxicity of NK cell and induce proliferation cells.

Front 79

What mediators activate NK cells

Back 79

IFNalfa/beta, IL-12 and TNF-alfa

Front 80

function IFNalfa/beta on NK

Back 80

development of the cells' killer functions

Front 81

function IL-12 on NK

Back 81

IFN-gamma release to activate macrophage. and then macrophage activates T cell.

so IFN-gamma of NK induces adaptive response.

Hint 81

IFN-gamma = type 2 interferon.