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IHL Exam 2 > Cytokines of adaptive immunity > Flashcards

Cytokines of adaptive immunity Flashcards

1
Q

IL-2

A

TH2 subset

mediates growth, survival and differentiation of T lymphocytes by exerting anti-apoptotic function by activating Bcl-2 (mitochondria surface)

induces synthesis of cyclins and induces degradation of p27 (cdK inhibitor so can’t slow down cell cycle)

necessary for survival of Reg t cells

stimulates NK cells

Stimulates Ab production

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2
Q

what produces IL-2

A

CD4+ T cells (T helper cells)

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3
Q

what activates IL-2

A

Antigen presentation and costimulators

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4
Q

What are the cytokines of the TH2 subset

A

IL-2

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5
Q

what is CD8+

A

cytotoxic cells

destroy cells

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6
Q

IL-4

A

of the TH2 subset

stimulates differentation of CD4 to TH2
inhibits TH1 differentiation

defense against helminthic or arthropod infection (mast cells and eosinophils)

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7
Q

when do allergies occur

A

When IL-4 stimulates IgE production

IgE then goes on to help eosinophils and mast cells degranulate in the ABSENCE of a microorganism (so happening unusually)

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8
Q

Systemic activities of IL-4

A

Allergies

Fibrosis

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9
Q

How does IL-4 and IL-13 stimulate fibrosis?

A

induces arginase expression in macrophages

arginase diminishes activity of NO synthase

NO synthase promotes extravasation/inflammation normally

so decreased level of this will promote “wound healing” type of response –> leading to fibrosis

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10
Q

why do we want fibrosis with parasites?

A

collagen deposition helps to isolate the parasite so they can’t release toxins and damage tissues

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11
Q

what makes IL-4

A

TH2 subset

Mast cells

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12
Q

IL-5

A

Functions:

  • Activator of eosinophils
  • stimulates B cells to proliferate and produce IgA
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13
Q

Why is it important for IL-5 to stimulate B cells to produce IgA

A

Because IgA is mostly responsible for mucosal immunity

often parasites are associated with mucosal surfaces

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14
Q

what produces IL-5

A

TH2

activated mast cells

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15
Q

IL-13

A

TH2 subset cytokine
has shared effects with IL-4

this is the chemical signal that allows us to get somatic tissues to respond to our TH2 response
(promotes extravasation)

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16
Q

what produces IL-13

A

CD4+ T helper cells (TH2)

can also be produced by (minor contribution):

  • NK cells and TH1 cells during early phase allergic response
  • basophils and eosinophils
17
Q

Where are receptors for IL-13

A 
B cells
mononuclear phagocytes
Dendritic cells
Eosinophils
Basophils
Endothelial cells
Bronchial epithelial
NOT IN T CELLS
18
Q

Clinical application of IL-13

A

Promotes Fibrosis

  • arginase
  • induces TGF-beta
  • chronic asthma (one receptor is on bronchial epithelial)

Induces mucus production
-bronchial epithelia

Induces IgE class switching in B cells

Induces inflammation

  • extravasation
  • VCAM-1 on endothelial cells
19
Q

IFN-gamma

A

macrophage activating cytokine

TH1 subset

produced in response to presence of intracellular microbes

20
Q

what produces IFN-gamma

A

CD4+ T cells (TH1 subset)

CD8+ T cells

NK cells

21
Q

what stimulates production of IFN-gamma

A

IL-12

22
Q

How does the body kill microbes in the cytoplasm of cells?

A

CD8+ (cytotoxic killer cell) actually kills the entire infected cell

macrophage undergoes apoptosis

23
Q

How does the body kill microbes contained in vesicles inside the cell?

A

Macrophages are stimulated by IFN-gamma, which induces Reactive oxygen and NO within lysosomes to destroy microbes

24
Q

whenever we have a TH1 type of reaction we want to reduce eosinophilic reaction. How is this done?

A

IFN-gamma inhibits IgE

25
Q

Functions of IFN-gamma

A

Promotes TH1 differentiation (with IL-12)

Promotes B cells to switch to IgG

  • activates complement
  • activates phagocytes to opsonize microbes
  • inhibits IgE (no more eosinophil)

Stimulates antigen processing on APC’s
-induce MHCI and II expression

Promotes extravasation (TNF)

26
Q

What stimulates IL-12

A

whenever cell surface markers are found on cells

IL-12 then goes on to stimulate TH1 subset–> producing IFN-gamma

27
Q

TGF-Beta

A

Activity dependent of timing and whether or not its systemic or local

Inhibits proliferation of lymphocytes and leukocytes

Counteracts the effects of inflammatory cytokines on neutrophils and endothelial

Stimulates healing (fibrosis, angiogenesis)

Stimulates B cells to produce IgA (mucosal immunity)

28
Q

what produces TGF-beta

A

Antigen-stimulated T cells

LPS-activated phagocytes

Regulatory T cells

29
Q

what is opsonization

A

a pathogen is marked for ingestion and destruction

usually involves the binding of an opsonin (antibody) to a receptor on the pathogens cell membrane

this attracts phagocytes which then bind and eat up the pathogen

can also happen with IgG where the pathogen does not need to be ingested/phagocytosed, rather IgG triggers a release of lysis products from the immune effector cell (macrophage, eosinohpil, NK cell, etc)

30
Q

Case study–> positive intracellular virus infection.
liver biopsy reveals chronic inflammation and fibrotic tissue changes

which cell type is most likely responsible for the deposition of collagen?

A

macrophages

which are produced by TH2 subset

31
Q

what is innate response to a virus

A

IL-12–> leads to activation of TH1 helper cells producing IFN-gamma

Type I interferons

32
Q

what if the innate response doesn’t clear up virus or extracellular infection….

A

after TH1 response, then switch response to TH2
this is long-term response

TH2 pathway lead to fibrotic response from macrophages and fibroblasts

33
Q

Classical response to innate and TH1 responses of macrophages do….

A

antigen presentation

phagocytosis

induction of NO synthase–> assisting in inflammatory process and recruitment

34
Q

Macrophages alternatively activated do what…

A

Induce fibrosis

expresses arginase–> inhibit NO synthase

no longer properly do phagocytosis

inhibit TH1 cell response

35
Q 
Case study
9 year old
history of allergies/asthma
physician--> the persistence of an initial infectious stimulus may have skewed the tissue's response towards fibrosis/mucus production/inflammation through extravasation/myofibroblasts
what cytokine is involved?
A

IL-13

first you have your initial stimulus which is seen as persistent infectious agent

transition to TH2 cytokine response

Secondary stimulus then exacerbates fibrotic response

36
Q

Myofibroblasts

A

produce alpha-smooth muscle actin

this causes constriction in the lungs

IHL Exam 2 (14 decks)

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