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Immunology > Lec 4: Basics of Cell-to-Cell communication > Flashcards

Lec 4: Basics of Cell-to-Cell communication Flashcards

1
Q

How do immune cells communicate at a distance

A

Secretion fo proteins, hormones. Note here that concept of diffusion applies

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2
Q

Classes of Cytokine effects

A

soluble secreted proteins that act in an autocrine or paracrine manner

Pleiotrophy

Redundancy

Synergy

Antagonism

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3
Q

Pleiotrophy

A

induced varied responses in the target cell

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4
Q

Redundancy

A

different cytokines induce the same response

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5
Q

Synegry

A

cytokines cooperate in inducing a specific response

IFN for example (multiple can converge and boost a given signal)

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6
Q

Antagonism

A

cytokine blocks the activity of another cytokine

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7
Q

Why is the diversity of cytokine folds important

A

many conformations implies

different diffusion rates

different specificities

different regulators

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8
Q

what do cytokines depend on

A

transcription factors, signalling protiens present and epigenetic effects

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9
Q

why are cytokines benificial

A

for modulation of the immune response

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10
Q

Why is the redundancy of cytokines important

A

incase on cytokine does not work, we can maintain and immune response even with a partial loss

can boost a given signal (this is a synergistic effect and coordination)

cross talk

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11
Q

Why is antagonism important

A

what to dampen the signal at the end

also allows different tissues to react in different ways (reversal of immune response)

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12
Q

Can a single cytokine bind to multiple receptors

A

yes

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13
Q

what are the 5 classes of cytokine receptors

A

Ig-type ectodomain

TNF homotrimeric ectodomain

Cytokine Type 1 receptors (core ectodomain), can have other domains

Cytokine TYpe 2 receptors (core ectodomain), can have other domains

Chemokine receptors (typical and atypical)

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14
Q

Paracrine vs autocrine

A

Paracrine signaling: a cell targets a nearby cell (one not attached by gap junctions). The image shows a signaling molecule produced by one cell diffusing a short distance to a neighboring cell. Autocrine signaling: a cell targets itself, releasing a signal that can bind to receptors on its own surface.

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15
Q

Paracrine vs Autocrine

A

Paracrine signaling: a cell targets a nearby cell (one not attached by gap junctions). The image shows a signaling molecule produced by one cell diffusing a short distance to a neighboring cell. Autocrine signaling: a cell targets itself, releasing a signal that can bind to receptors on its own surface.

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16
Q

IL2 and IL15

A

IL2 and IL15 are essential cytokines mediating cell proliferation (IL2 is especially important in clonal expansion)

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17
Q

STAT5

A

STAT5 binds genes associated with cell proliferation, apoptosis, differentiation and inflamation

big driver of proliferation and apoptosis

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18
Q

How do antigen presenting cells change the flavour// activate a given T-cell

A

In this order

MHC
CO-stimulation (additional signal cascades)
Cytokine secretion

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19
Q

How are chemokines classified

A

divided into subfamilies on the basis of the presence of as conserved cysteine motif in their mature sequenses

are folded together by cysteine bridges

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20
Q

Pleiotrophic effects of chemokines

A

Extensive ligand promiscuity in the chemokine receptor family, and many chemokines can bind to multiple receptors

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21
Q

classes of chemokines

A

C
CC
CXC
CX3C

see slides for diagram

22
Q

Typical chemokine receptors

A

containing a seven-transmembrane domain

G protein-coupled chemotactic receptors

conserved DRYLAIV motif (AA sequence)

cell migration

23
Q

Atypical chemokine receptors (ACKRs)

A

predicted seven transmembrane domain structure

do not signal through G proteins and lack chemotactic activity

substitutions in the DRYLAIV domain

Signalling via beta-arrestin leads to chemokine internalization

24
Q

What is the purpose of beta-arrestin signaling

A

Signaling via beta-arrestin leads to chemokine internalization = ANTAGONISM

ligand scavenging and degredations

chemokine trafficking

control inflammatory and immune responses

25
Q

nomenclature for typical chemokines receptors

A

CCL and CXCL

26
Q

nomenclature for Atypical chemokines receptors

A

ACKR

27
Q

how do atypical chemokine receptors help control infammation

A

they help to trap excess chemokine

erythrocytes can act as a buffer for excess serum chemokines

protection against excessive cytokine storms or chronic inflammation

28
Q

Viruses can usurp cytokine signalling

A

some viruses encode protiens that mimic host cytokines, chemokines and their receptors

Viral mimics do not have sequence similarity to host proteins, yet possess similar function

29
Q

what do you notice about the types of chemokines herpesviruse mimics

A

immunosupression

IL6 reduces the inflammatory response and chemokine signalling

30
Q

Viralkines

A

Mimics cytokine, chemokine, or chemokine receptors

interupt, mimic or distrupt host signalling cascades

Ep-barr secretion of IL10 to suppress adaptive and innate immune responses

31
Q

What kind of extracellular signals do cells use do communicate

A

Secretion of cytokines// proteins as well as hormones to induce immunocompetent (diffuses into cells)

The can also secrete exosomes

32
Q

Extracellular vesicles

A

delivery of bioactive macromolecules

enclosed in a lipid bilayer, variable composition

can enhance or supress immune activites

33
Q

Why are extracellular vesicles so important when it comes to cell signalling

A

They contain a ton of information abot the cell that secreted them

Surface markers, DNA, proteasome etc…

34
Q

What are the two types of extracellular vesicles

A

exosomes and microvesicles

35
Q

How does loss of integrety// secreation// membrane blebbing occur?

A

increase in temperature, and infection, toxins high osmotic stress etc

36
Q

Necrosis// Necrotic Cell Death

A

aka cell lysis NOT apoptosis (dis is more violent)

membrane rupture makes apoptotic blebbs which are little packets that may be degraded

huge inflamatory response

37
Q

Apoptotic bodies

A

Small little fragments to be eaten by macrophages

Cell contents not released, no inflamatory response

contain valuable information about the cells death

38
Q

Biogeneisis of exosomes

A

A modified endosome, the intracellular components of these can be controlled

Derived from MBV (multivesicular bodies) which fuse with the plasma membrane and release intraluminal vesicles as exosomes

30-100nm

39
Q

Biogenesis of microvesicles

A

generated from budding from the plasma membrane

lil scoops of a sample of the cytoplasm

30-2000nm

40
Q

Dendridic cells and Extracellular vesicles

A

Dendritic cells may engulf important anitgens or signalling moleucles then secreate them in extracellular vesicles to a variety of immune cells

may lead to inflammatory responses and or immune cell activation

41
Q

Diffusion of PRR to other cell types

A

activation of other non-infected cells

super important in exosomes

42
Q

Exosome secretion during infection

A

exosomes containing antigens derived from pathogens can helpp activate the imune system through PAMPs and cross-priming DC antigen presentation

also can have immunosuppressive effects

43
Q

Group cytokines and chemokines based on their strucutre and receptors

A

Chemokines:
cysteine bridges in 4 groups, C, CC, CXC and CX3C chemokines which can bind to either typical or atypical receptors. Chemokines exhibit extreme promiscuity when it comes to their receptors (they can often bind many)

Cytokines:
Conformationally very different which lead to variations of specificity, difffusion and regulation. They bind to 5 different types of receptors (Ig-type, TNF homotrimeric, Cytokine type 1, cytokine type 2, chemokine). Usually again, a given cytokine can bind multiple receptors

44
Q

Compare and contrast the actions of cytokines and chemokines

A

A chemokine is a cytokine that specificaally induces motility towards a site of inflamation

45
Q

Explain the importance of Cytokine-based communication in terms of pleiotrophy

A

here communication is important because pleiotrophy of target cell means different cells with respond differently to a given cytokine.

This is due top variations of a cells given receptors, epigenetics, proteasome, transcription factors, and constituents of the signal transduction cascade

46
Q

Explain the importance of Cytokine-based communication in terms of redundacy

A

Redundancy is important because just incase their is a mutation, or infection or simply the cell doesn’t have a given receptor the end result will still get triggered

issa good back up plan

47
Q

Explain the importance of Cytokine-based communication in terms of Synergy

A

Coordination, and cooperation and crosstalk to boost signals

for example, IFN signals boost each other

48
Q

Explain the importance of Cytokine-based communication in terms of antagonism

A

Imporant when you want to silence a cascade before it gets out of control or simply because you dont what that signal in a given cell type or tissue

49
Q

What is the importance of extracellular vesicles in immune communication and signalling

A

Allows a “controlled” diffusion of lysed cell components among the blood stream or lymph to activate immune cells (this is jsut one example = a dendritic cell).

membrane vesicles give a good idea of what happened at a given site of infection.

50
Q

MAPK

A

A mitogen-activated protein kinase is a type of protein kinase that is specific to the amino acids serine and threonine. MAPKs are involved in directing cellular responses to a diverse array of stimuli, such as mitogens, osmotic stress, heat shock and proinflammatory cytokines

Immunology (23 decks)

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