Immunology 9: Host Response To Infection

Front 1

what kind of response do you want for an intracellular bacteria infection?

Back 1

Th1 b/c they stimulate IFN gamma which stimulates macrophages

Front 2

protective immunity of blood/interstitial space/lymph infection

Back 2

antibodies
complement
phagocytosis
neutralization

Front 3

protective immunity for cytoplasm infection

Back 3

cytotoxic T cells
NK cells
Th1 cells

Front 4

protective immunity for vesicular infection

Back 4

T cell and NK cell dependent macrophage activation

Front 5

protective immunity from toxins?

Back 5

antibody. but b/c they're proteins, want T cell help- primarily an IgG response, not IgM

Front 6

protection against infection- innate,

Back 6

1. virus infects cell
2. cells recognize virus b/c of TLR
3. cell releases type I IFN which binds and activates cells nearby
4. cell dies

Front 7

protection against infection- adaptive

Back 7

B cell makes antibody which neutralizes viruses by blocking ability to bind to to particular target cell

Front 8

eradication of established infection-innate

Back 8

NK cells recognize infected cells that lack MHC Class I. KILL

Front 9

eradication of esetablised infection- adaptive

Back 9

CD8 cell recognizes infected cell with MHC class I --> Death

Front 10

IFN alpha and beta

Back 10

innate immunity
inhibition of protein syntehsis

Front 11

where do T cells interact with APCs?

Back 11

cortex of lymph node

Front 12

where do T cells get activated?

Back 12

lymph node

Front 13

adhesion expression on T cell change from naive to effector

Back 13

L-selectin- CD34 --> LFA-1 ICAM-1

Front 14

what produces IL-12?

Back 14

dendritic cells

Front 15

What stimulates production of IL-12

Back 15

chemokines: CCL3,4,5
prostoglandin E2
binding if TLR

Front 16

for a bacterial infection: between wt, knockout IL12, knockout IFNgamma, which is most extreme?

Back 16

IFN-gamma

Front 17

cooperation of CD4 and CD8 cells in infection

Back 17

CD4 cell makes IFN-gamma which kills the bacteria in the phagolysosome while binding of CD8 kills the infected cell

Front 18

effect of antigen on T cell subset differentiation

Back 18

tightly binding antigen=> Th1
high peptide density

Front 19

can same protein stimulate both Th1 and Th2 cells? why?

Back 19

yes b/c most proteins have multiple epitopes

Front 20

1st wave of B cell- Th2 cell interactions

Back 20

B cells enter the T cell areas of secondary lymphoid tissue

B cells present antigen to Th2 cells

Th2 cells stimulate B cells to proliferate and mature into plasma cells

Front 21

2nd wave of Bcell-Th2 interactions

Back 21

B cells and Th2 cells migrate to the follicles where they proliferate, form germinal centers, and undergo somatic mutation leading to the selection of high affinity Ig and leave to become plasma cells

Front 22

5 ways antibodies defeat bacterial infection

Back 22

1. toxin neutralization- prevents toxin action
2. kill bactera directly through complement mediated lysis
3. opsonization and phagocytosis through C3b
4. C3a and C5a aid masst cell degranulation and increased vascular permeability leading to extravasation of lymphocytes and PMNs (granulocytes)

5. chemotaxis cause macropahges and granulocytes to come

Front 23

what type of antibody is associated with mucosal linings?

Back 23

IgA b/c stable at low pH and because it binds to secretory piece that allows it to dimerize and allos for transcytosis to occur

Front 24

for muscoal immunity, where are the lymphocytes activated?

Back 24

GALT

Front 25

trafficking of T cells

Back 25

naive lymphocytes enter Peyer's patch from blood

they are activated by antigen there and enter lymph to return to blood

they circulate in blood and enter all submucosal lymphoid tissue

Front 26

effector T cell migration to gut

Back 26

effector T cells with L selectin and alpha4beta7 integrin -- MadCam-1 of endothelium

then they go from the endothelium to the small/large intestine b/c gut epithelial cells express chemokines

Front 27

response to enteric pathogens

Back 27

kill M cells which lead to engagemtn of TLR5 and TLR4 on gut epithelial cells which stimulates an inflammatory reaction via NKkappaB

they can directly enter dendritic cells which activates an inflammatory response

Front 28

inflammatory response to enteric pathogens is driven by

Back 28

production of chemmokines and upregulation of chemokine receptors

Front 29

immune response to worm

Back 29

activate eosinophils through binding of IgE to mast cell which result in the release of proteins to kill worms

Front 30

what does protective immunity consist of?

Back 30

preformed antibodies and existing effector T cells

Front 31

B cell memory consists of 2 factors

Back 31

increase in frequency of antigen specific B cells

increase in affinity and amt of immunoglobulin made for antigen

Front 32

Blimp-1

Back 32

represses B cell proliferation, germinal center function

upregulates genes involve in Ig secretory pathway

Front 33

what cytokines are necessary for T memory cell survival

Back 33

IL-7 and IL15

Front 34

2 categories of memory cells

Back 34

effector
central

Front 35

central memory cells

Back 35

undergo self reneval via homeostatic proliferation. <-- doesn't happen with effector cells

Front 36

original antigenic sin

Back 36

shows that initial exposure to pathogen can restirct future immune response to different strains of the same pathogen

but response is naive if there is no sharing of antigenic epitopes

Front 37

mechanisms of immune evasion by viruses

Back 37

inhibition of humoral immunity
virally encoded complement receptor
blocks complement mediated effector pathways
herpes simplex

blocking of antigen processing and presentation
inhibition of MHC Class I expression
impairs recognition of infected cells by cytotoxic T cells
cytomegalovirus

Front 38

removal of class I MHC from ER is done by

Back 38

CMV

Front 39

Block in TAP transport is done by

Back 39

HSV

Front 40

2 types of antigenic variation in viruses

Back 40

antigenic drift
antigenic shift

Front 41

antigenic drift

Back 41

mutations in epitopes make it so that neutralizing antibody can no longer bind

Front 42

antigenic shift

Back 42

RNA exhcange with other viral strains

Front 43

superantigen

Back 43

stimulates MHC ClassII and TCR and leads to massive cytokine produciton --> shock

25% of T cells involved then deletd

Front 44

mechanisms of immune evasion for bacteria (2)

Back 44

antigenic variation
inhibition of phagolysosome formation

Front 45

mechanisms of immune evaiosn for parasites (2)

Back 45

antigenic variation
acquired resistance to complement, cytolytic T lymphocyte