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review class Flashcards

1
Q

how do IFN responses promote a feed-forward loop

4

A

FDCs are the main secreters of IFN

IFN increase the cytotoxicity of CTLs, which will kill infected cells and increase more local debris which can be utaken by APCs

maybe talk about first and second wave IFN signalling here?? idkidk

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2
Q

How does the innate immune system react to PRR activaiton

A 
NFkb
IRF
IFNS
pro-inflammatory cytokines
ISGs (and resttriction factors)
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3
Q

First wave IFN

A

happens inside an infected cell
when a cell is infected
PRR activaiton

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4
Q

second wave IFN

A

ifn produciton in initial infected cell and neighbouring cells

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5
Q

IRF3

A

in the cytoplasm, when it dimerizes it activates the transcription of interferons alpha and beta, as well as other interferon-induced genes.[8]

IRF3 plays an important role in the innate immune system’s response to viral infection.

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6
Q

IRF7

A

IRF7 regulates many interferon-alpha genes.[5] Constitutive expression of IRF7 is largely restricted to lymphoid tissue, largely plasmacytoid dendritic cells,

has been shown to play a role in the transcriptional activation of virus-inducible cellular genes, including the type I interferon genes

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7
Q

Outcomes of IFN signalling cascades

A

???

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8
Q

Redundancy

A

multiple moleucles have the same effects

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9
Q

Exosomes

how do they stimulate immunity

2

A

extracellular vesicles deliver bioactive molecules
-> can supress or activate immune activities

effect on APC activation
Effect of Cytokines
Effect on cellular cytotoxicity

all depends on the cargo they hold
(look at examples in the text)

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10
Q

Which forms of cell death drive inflammarion

3

which drive inflammation and which dont

A

NETosis, Necrosis = inflammaotry

Autophagy and apoptisis are non-inflammatory

Apoptotic bodies taken up by phagocytes
Autphagy = self degredations and autophaic grannules uptaken by phagocytes

necrosis lysis and release damps
pyrotosis releases cellular contents

silent clearence of apoptotic bodies
cell lysis drive prr activation through damps

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11
Q

phagocytes clear apoptotic bodies

A

two stages:

recruitment and engulfment

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12
Q

Compare and contrast the function of neutrophils and macrophages in the progress and resolution of inflammation

A

????

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13
Q

What is NETosis

3

A

PROINFLAMMATORY

utalization of DNA as a trap for pathogens

decondensation of chromatin
ruptures the neutrophile or small release of DNA

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14
Q

What is NETosis

3

A

PROINFLAMMATORY

utalization of DNA as a trap for pathogens

decondensation of chromatin
ruptures the neutrophile or small release of DNA

has pathogen toxin grannules inside the chromatin

benifit = trap and has antimicrobial enz

cons= proinflammatory and may lead to autoimmunity

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15
Q

what is in NETs

A

granule protiens bind extruded DNA

elastase and cathepsis G

myeloperoxidase

DNA and Histones

prevents dissemination of microbes

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16
Q

Dendritic cells, PRR activaiton and antigen presentation

innate immune response and apc, trafficking and maturation

6

A

???

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17
Q

antigen processing in DC

A

MHC1 present endogenous peptides (intracellular)
= self proteins or viral and or cancer peptides
=loaded into the ER by tap proteins after degredation by the proteasome
=loaded onto the MHC1
=recognized by CD8+ T cells as well as NK cells (recall this is an inhibitory signal for these bad bois)
-> this happens in all cells of the body
-> essential such that cytotoxic cells can recognize strange or the lack of self peptides
-> smaller peptides (closed pocket)

MHC2 present exogenous peptides
-> expressed only on APCS like DCs, monocytes, macrophages, B cells and eosinophils
=brought into the endosome where is it digested
=vesicle fused with another that had MHC2 within, exchage with CLIP and then presented to CD4+ cells
-> biggerpeptides becasue there is an open pocket

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18
Q

cross presentaion

A

in autophagy
= consumption of peptides and transfer to and MHC 2

DC can uptake exogenous antigen and present it to a type 1 pathway
= exogenous antigen to a ensogenous pathways

only happens in specific cell types
-CD8+ DC

CD8+ T cells are not the same as CD*+_ DC

19
Q

What activates a DC

A

PRR activaiton leads to increased antigen uptake and processing
=> DC starts to mature and presents antigen on it surfaces, presentation of co-stimulatory ligands and the capacity to activate a T cell

20
Q

stages of DC activaiotn

A

Myeloid vs plasmacytois DC

first stage is differentation from their precursors

seconds stages is increased rate of antigen uptake

thrid is antigen processing

fourth is phenotype maturation
=cell surface markers are CD CD80/86, CD83

functional maturation
=the capacity for a DC to actually activate a T cell
=secretion of cytokines like IL-13 and TNF

21
Q

`DC migration to the lymph node

A

diffedrend DCs resides as teh barrier sites
=skin and mucosla surfaces

upregulation of migratory capacity after antigen uptake
= upreg of CCR7 to home towards a lymph node ( just like the T cells do)

no longer uptakes any new antigen

snap shot of the site of infection

22
Q

how do you activate a Th17 cell

3

A

three signal activaiotn

want to expand and differentie

Il-2 for proliferation (clonal expansion) and polarizing cytokines

Th17 requires IL-6 and TGHbeta causes the upreguatio of RORgt which causes differentaiton to an effector cell
= leads to the secreation of mediatiors Il-17A, IL-17F and Il-22

23
Q

why is clonal expansion so important

A

multiple cells that all share the same specificity to a given MHC-peptide complex

lots of effectors targeted to the same outcome

more than one cell is requred to fight an infection

not all cells surrvive after an infeciton
=we need memory cell!!

24
Q

What motivates cells to traffic to organs and move into vessicles

know where cells develop from, and which organs the cell move to and traffic inbetween

3

A

chapter 14
511-533

go over those figures boisss

thymocytes reside in the thymus for 4-5 days undergoing negative selection

25
Q

CCR7 and S1PR1

A

CCR7 is essential for T cell homing to the lyumph nodes and the thymus

S1PR1 sensitivity recruits T cells abck to circulation and lymph

more CCR7 = will move to the lymph node
more S1PR1 = more likley to move towards circulation

26
Q

four key steps of immune cell extravasion from vasculatore into tissues

A

rollin, activaiton, arrest/ adhesion/ and transmigration

27
Q

four key steps of immune cell extravasion from vasculatore into tissues

A

rollin, activaiton, arrest/ adhesion/ and transmigration

28
Q

what is the fuction of cTECs and MTECs

4

A

purple thymus slides

know potive and negative selection in the thymus

cTECS
postive
=T cells need to recognize selfg MHC, otherwise if they dont revognize MHC they are usless
(because they need to see peptides in the context of MHC)

negative
=if they recognize MHC too strongly in the absene of peptides they are killed off because they are autoreactive

mTECS
= special because they express the transcription factore AIRE and express tissue specific antigen
=loses up chroimatin and allows the transcription of normally silenced genes

29
Q

Tregs

A

autoreactive

bind MHC stoo strongly

help to supress immune response of other immune cells

help to maintain tolerance

30
Q

How does antigen traffic through a lymph node

4

A

there is two ways

free flowing and fDCs

31
Q

Organization of lymph nodes

A

??

32
Q

Where does antigen enter the lymph node

A

via and afferent lymph and enter the B cell zone

is uptaked by resident Subcapular sinus macrophaged and fDCS

B cell interact with intake antigen through their BcR and processed antigen like T cells

33
Q

Lymphocyte migration alone the firbroblast reticular cells

A

guided by 3d netword

FRC network surround the HEVs and naive T cells exit from HEVs
________IDKk

34
Q

What are the products of an effective GC response

4

A

what the inital cells that are aftivation to undergo mutation = affintiy maturation

35
Q

classical T cell B cell interactions

A

Tfh cells are CD4 that provide something

36
Q

classical T cell B cell interactions

A

Tfh cells are CD4 that provide something

?????

37
Q

AID

A

important enzymne in SHM

mutates cytosine to uracil
= leads to DNA repair and mutation in the DNA sequence

trial and error processs

38
Q

differentiate light and dark zone of the GC

A

do it

39
Q

What does it mean to be a memory cell

3

A

what happens after the collapse of a immune response

Memory cells live

they are the first cells to be activated upon secondaary exposure to an antigen

differnt type of memory cells

T effector
Tem

CCR7 long lived
Trm memory celkls

not all reside in the same areas, lifespans or capacity to become memory cells

40
Q

Chemokine receptors

A

Typical vs atypical receptores

typical = DRYLAV motif, and are G protein coupled receptors

atypical =substituiton int he DRYLAVmotif and are not G protien coupled receptors
= can help to scavengw chemokines and are immunomodulatory

41
Q

Complement proteins

A

MAC complex

forms holes and pores in the target cell membrane

leads to lysis of the target cell

Chapter 12 437-438

know the purpose of the signalling cascade
-> and what C1 does as well as outcomes

42
Q

C5a

A

is a chemoattractant for inflammatory cells and is a part of the complement cascade

43
Q

antibody mediated immune reactions

A

know three effector mechanism for the final

neutralization, agglutination, precipitation

complemetn fixation, opsonizationa nd actiaviton of NK cells

Immunology (23 decks)

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