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PDAT4 > 12 - Cytokines > Flashcards

12 - Cytokines Flashcards

1
Q

General CYTOKINE Traits

A

Are NOT stored
are rapidly synthesized & secreted after stimulation

Cellular Responses consist of:
Changes in GENE EXPRESSION
VVV
New Functions / PROLIFERATION of target cell

  • EXCEPTIONS:*
  • *Chemokines / TNF**
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2
Q

Which CYTOKINES do NOT result in
New Functions or Proliferation
after gene expression?

A

CHEMOKINES
induce motility

TNF
induce apoptosis

do NOT need activation of NEW PROTEINS
SUFFICICIENT ON THEIR OWN

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3
Q

Regulation of Cytokines

A

QUANITITY of cytokine Produced

EXPRESSION** or **DOWN-REGULATION
of Cytokine Receptors

Low Affinity Receptors
are found on MOST CELLS, in LOW QUANTITY

High Affinity Receptors
are expressed on ANTIGEN ACTIVATED cells

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4
Q

3 Types of CYTOKINE action

A

Autocrine
Act on SELF

Paracrine
Acts on NEARBY cell

Endocrine
Passes through CIRCULATION –> DISTANT CELL

IL-2 DOES ALL 3

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5
Q

What is PLEIOTROPY?

A

Pleiotropy

ONE CYTOKINE can act on MULTIPLE CELL TYPES

DIFFERENTLY

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6
Q

What is REDUNDANCY?

A

Redundency

MULTIPLE CYTOKINES
have the
SAME EFFECT** & use the **SAME SIGNALING SUBUNITS

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7
Q

Synergy / Antagonism
properties of Cytokines

A

Synergy
cytokines act together –> induce something

  • *Antagonism**
  • another cytokine** –> *_antagonizes action of another_
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8
Q

How do we CLASSIFY CYTOKINES?

A

BY THEIR ACTION

Functional Classification of Cytokines

Mediators & Regulators of INNATE & ADAPTIVE IMMUNITY

Stimulators of Hematopoeiesis

Chemokines

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9
Q

What are the PRIMARY PRODUCERS of
Cytokines of the INNATE IMMUNE SYSTEM?

A

MONONUCLEAR PHAGOCYTES
Dendritic Cells + Macrophages

Also by,
Endothelial + Epithelial Cells

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10
Q

What do these cytokines MEDIATE & REGULATE?

TNF-A

IL-1 // IL-10 // IL-12

INF-A + INF-B

Chemokines

A

INNATE IMMUNE SYSTEM

Produced primarily by:
Mononuclear Phagocytes = Dendritic cells + Macrophages

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11
Q

Which Cytokine?

Mediator of ACUTE INFLAMMATORY RESPONSE
to GRAM (-) Bacteria & other microbes

Induces INFLAMMATION
in an effor to limit spread of infection

Responsible for many
systemic complications of severe INFECTION

A

TNF-A

Mediator & Regulator of INNATE IMMUNITY

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12
Q

Low Quantities of TNF-A cause what?

TNF-A Biologic Actions

A

LOCAL INFLAMMATION

Neutrophil Activation –> Chemokine Production

Endothelial cells activated to
secrete chemokines + adhesion molecules

some Apoptosis

Increased Vascular permeability / Redness / Swellin
Inflammation

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13
Q

MODERATE Quantities of TNF-A cause what?

TNF-A Biologic Actions

A

SYSTEMIC EFFECTS

Brain –> produces FEVER

Hepatocytes produce Acute Phase Proteins

Bone marrow leukocyte production is increased

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14
Q

HIGH QUANTITIES of TNF-A cause what?

TNF-A Biologic Actions

A

SEPTIC SHOCK

Heart -> low output due to inhibition of myocardial contractility

Vascular endothelium

HypoGlycemia

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15
Q

Which Cytokine?

Pro-Inflammatory with TNF-Alpha

@Low Concentrations
local inflammation

@HIGH concentrations
Pyrogen / Cachexia / Acute Phase Proteins Secreted

A

IL-1

Secreted by Activated Macrophages

Mediator & Regulator of INNATE IMMUNITY

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16
Q
  • *IL-1 + TNF-A**
  • *Functions Together**

Mediator & Regulator of INNATE IMMUNITY

A

they make ENDOTHELIAL CELLS:

  • *LEAKY to fluids**
  • -> influx of plasma w/ AB’s
  • *STICKY for leukocytes**
  • -> influx of neutrophils –> monoctes/lymphocytes
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17
Q

DIFFERENCES between IL-1 and TNF-A

Mediator & Regulator of INNATE IMMUNITY

A

IL-1

cannot cause cell APOPTOSIS

cannot cause SHOCK by itself

binds DIFFERENT RECEPTOR, but produces a similar effect

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18
Q

What Cytokine?

INDUCER of ADAPTIVE Immune response
VVV
Stimulates DIFFERENTIATION of
Th -> Th1 (produce INF-y) –> macrophage activation
&
Enhances Cytolytic fxn of Activated CD8+ T-cells
–> LYSIS of infected cell

Principle mediator of:
EARLY INNATE IMMUNE RESPONSE

A

IL-12
Th –> Th1 producing TNF-y
macrophage activation -> kill phagocytosed microes
Enhance CD8+ Tc
lysis of infected cell

from activated macrophages + dendritic cells

Mediator & Regulator of INNATE IMMUNITY

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19
Q

What Cytokine?

INHIBITOR of host immune responsed involving macrophages
INHIBITS Cellular Immunity
in favor of HUMORAL RESPONSE

INHIBITS production of IL-2** & **TNF-a
by activated macrophages

INHIBITS expression of Costimulators** & **MHC
by macrophages

A

IL-10

From
Th2 cells + late stage macrophages

Mediator & Regulator of INNATE IMMUNITY

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20
Q

What Cytokine?

Interfere with VIRAL REPLICATION
response to dsRNA

LEUKOCYTE INTERFERON

Major source is
Mononuclear Phagocytes & Viral-Infected Cells

A

INF-a

Mediator & Regulator of INNATE IMMUNITY

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21
Q

What Cytokine?

Interfere with Viral Replication
response to dsRNA

FIBROBLAST INTERFERON

Major source:
Fibroblast + Virally Infected Cells

A

INF-B

fibroBlast interferon

Mediator & Regulator of INNATE IMMUNITY

22
Q

4 Main Functions of

INF-A + INF-B

A

Both Bind SAME RECEPTOR & Ilicit SIMILAR BIOLOGIC RESPONSE

Induce Resistance
to viral replication in all cells

Increase MHC1** + **Antigen presentation

Activate Dendritic Cells + Macrophages

Activate NK Cells
to kill virus-infected cells

23
Q

Which Cytokine

Enlist ASSISTANCE from ADAPTIVE IMMUNE SYSTEM?

A

IL-12

Th0 -> Th1 differentiation
Th1 –> INFy produciton

Enhance CytoLYTIC Fxn of CD8+ Tcytotxic cells

24
Q

What Cytokine

INHIBITS / STOPS the INNATE/CELLULAR RESPONSE

A

IL-10

Inhibits production of
IL-12 & TNF-A
by activated macrophages

Inhibits expression of
Costimulators + MHC
by macrophages

25
Q

What Type of Cytokines?

IL-2 // IL-4 // IL-5

INF-y

TGF-B

A

Mediators & Regulators of
ADAPTIVE IMMUNITY

26
Q

What Cytokine?

Growth Factor for Ag-stimulate T-cells
responsible for T-Cell Clonal EXPANSION after AG recognition

  • *Autocrine/Paracrine Effect** on:
  • *T-Cell proliferation / NK activation / B-Cell Proliferation**

Promotes Cell-Cycle Progression

High Concentration –> APOPTOTIC DEATH of
AG-Activated T-cells

A

IL-2

from Th0 & Th1

Naive T-cell + IL-2 = Th0

Mediators & Regulators of
ADAPTIVE IMMUNITY

27
Q

What Cytokine?

Major Stimulus for 
**_IgE AB class switching_**

*Antagonizes* the Macrophage-Activating Effects of INF-y
–> inhibits cell mediated immunity

Major stimulus for differentiation of

  • *Th0 –> Th2**
  • -> Activation of B-cells
A

IL-4

From Th2 Cells

Mediators & Regulators of
ADAPTIVE IMMUNITY

28
Q

What Cytokine?

Major Stimulus for:
B-Cell Differentiation
&
Class Switching

Activates EOSINOPHILS
to destroy Parasite
IL-4 stimulates IgE –> opsonize parasites & binds eosinophils

A

IL-5

From Th2 Cells

Mediators & Regulators of
ADAPTIVE IMMUNITY

29
Q

What Cytokine?

PRINCIPAL:
MACROPHAGE ACTIVATING CYTOKINE
stimulates production of cytotoxic molecules by macrophages

INHIBITS PROLIFERATION of TH2 CELLS

Th0 -> Th1
Cell differentation

Stimulates
Expression of MHC & Costimulatory Molecules on APC

Isotype Switching
to opsonizing ABs in B-cells

A

INF-y

From
CD8+ Tcells & Th1 cells

Mediators & Regulators of
ADAPTIVE IMMUNITY

30
Q

Which cytokine is the

MACROPHAGE ACTIVATING CYTOKINE?

A

INF-y

Also
Inhibits proliferation of Th2 Cells

31
Q

INF-y

Main Functions & Image

A

Macrophage Activation

Isotype Switching -> Opsonizing AB’s

Th0 -> Th1

Inhbits Th2 Production

Increased MHC expression + Costimulatory Molecules on APC

32
Q

What Cytokine?

INHIBITORY CYTOKINE of ADAPTIVE IMMUNITY

Inhibits:
T-Cell Proliferation & effctor Fxn
B-Cell Proliferation
Macrophages

Promotes
IgA Isotype Switching in B-cells

A

TGF-B

Th0 -> TREG

From
Lymphocytes / macrophages / Platelets

Mediators & Regulators of
ADAPTIVE IMMUNITY

33
Q

What CYTOKINE?

Induces proliferation of T-REGULATORY CELLS
Tregs?

A

TGF-B

TREGS –> TGF-B & IL-10

Inhibitory Cytokine of Adaptive Immunty

34
Q

Key Differences
Between ADAPTIVE & INNATE Immunity Cytokines

chart

A
35
Q

Cytokines that are Stimulators of
HEMATOPOIESIS

A

Produced by:
Bone Marrow / Leukocytes

Promote:
Differentiation & Expansion of Bone Marrow Progenitor Cells

Drug Examples / Therapeutics:
Stem Cell Factor
M/G - CSF = Colony-Stimulating Factors
IL-3// IL-7//IL-5//IL-11

36
Q

What Cytokine/Drug is used to:
Stimulate RBC proliferation?

A

Erythropoietin

Epogen - Epoetin Alpha
Procrit

37
Q

What Cytokine/Drug is used to
INDUCE NEUTROPHIL PRODUCTION

A

G-CSF
G- Colony Stimulating Factors

Filgrastin = Neupogen

38
Q

What Cytokine/Drug is used to
INDUCE PLATELET PRODUCTION?

A

Thrombopoeietin

IL-11

39
Q

What is the MOST COMMON cytokine Receptor?

A

CLASS 1

Cytokine Receptor Hematopoietin

40
Q

Cytokine Receptors

A

Grouped Based on their:

  • *EXTERNAL DOMAINS**
  • signaling domains are often SHARED*

5 Major Families
Class 1 Cytokine Receptor hematopoietin
TNF Receptor
Class 2 Cytokine Receptor Interferon
IG Superfamily Receptor
Chemokine Receptor

41
Q

What type of PROPERTY of CYTOKINE RECEPTORS?

Association with the
SAME BETA SUBUNIT
required for
Signal Transduction

A

REDUNDANCY

42
Q

What type of PROPERTY of CYTOKINE RECEPTORS?

Competition of Ligand-binding chains
of
Different Receptors
for a
COMMON SUBUNIT

A

ANTAGONISM

43
Q

How is Cytokine Receptor Expression
HIGHLY REGULATED?

A

Inactive Cells
Express Low Affinity Receptors

Activated Cells
express HIGH affinity receptors

44
Q

IL-2 RECEPTOR

A

A-Chain = Cytokine Binding Component
Low Affinity, just binding

B + Y -Chain = Signal Transduction
Medium Affinity, beta + gamma

  • *All 3 = A+B+Y**
  • *complete signal transduction**,
  • *ONLY IN ACTIVATED T-CELLS**
45
Q

Cytokine Signal Transduction

IL-2

A
  • *IL-2 Receptor subunit** Gamma + Beta is associated with
  • *JAK**

Cytokine Binding --> JAK activation
VVV
docking sites for STATs
signal transduction to:
Growth + Proliferation + Survival
Transcription Regulation + Effector Differentiation

hard to regulate due to UBIQUITOUS = found everywhere

46
Q

What does a
Mutation in Class 1 Cytokine Receptor

GAMMA SUBUNIT

cause?

A

Class 1 is the MOST COMMON RECEPTOR

Gamma Subunit is necessary for Signal Transduction
VVV
Unable to TRANSMIT the CYTOKINE SIGNAL
VV
Increases SUSCEPTABILITY to INFECTIONS

47
Q

What Disease is caused by a

Enterotoxin derived from Gram Positive Bacteria

= SUPERANTIGEN

A

TOXIC SHOCK SYNDROME

48
Q

Toxic Shock Syndrome

A

Enterotoxin from Gram + bacteria
= SUPERANTIGEN

Crosslinks TCR + MHC2 on APC
resulting in over stimulation cytokine production by T-cells

Extremely high lvels of cytokines;
TNF-A** & **IL-1

Fever / Diarrhea / Clotting / HypoTension / shock
RARELY FATAL

49
Q

Bacterial Septic Shock

A

ENDOtoxin derived from Gram Negative bacteria

Bacterial LPS
Over-Stimulates Cytokine production by Macrophages

Extremely high levels of inflammator cytokines:
IL-1 & TNFa
(like Toxic Shock Syndrome)

Fever / blood clotting / rash / diarrhea / hypotension / shock
OFTEN FATAL

50
Q

Two Mechanisms of

Cytokine ANTGONISM / INHIBITION

A

PROTEINS produced by cells to l_ocally regulate cytokine activity_
Ex. IL-1 Receptor Agonist

Cytokine binding domain RELEASED
from cell surface as a result of
Enzymatic Cleavage
Ex- IL 2/4/6/7 + INFy + TNFb

51
Q

Cytokine Map

A
52
Q
A

PDAT4 (34 decks)

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