Exam 3: Immune deviation - TH1, TH2, TH17 Flashcards

1
Q

Master Transcription Factor for ILC 1 that drives TH1

A

T-bet

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2
Q

Master Transcription Factor for ILC2 that drives TH2

A

GATA-3

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3
Q

Master Transcription Factor for ILC3 that drives TH17

A

ROR-γT

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4
Q

Intracellular; Cell-mediated immunity (T. cell activation); inflammation; viruses, tuberculosis, leishmania

A

TH1

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5
Q

Extracellular; Humoral immunity; Allergies; WORMS; parasites;

A

TH2

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6
Q

What cytokines associated with TH1?

A

IL-12 from APC–> activates T-bet + TH1 cell–> IFN-γ

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7
Q

What cytokines associated with TH2?

A

IL-4 from various sources–> activated GATA-3 –> IL-4, IL-5, Il-13

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8
Q

Sources of IL-4?

A

Innate lymphoid cells (ILC2) is main source; Also –> Basophil, Eosinophil, NK T cell

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9
Q

What cytokines associated with TH17?

A

IL-23 + IL-1 from APC activate ROR-γT –> IL-17

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10
Q

Which type of response?

Tissue inflammation; Fungal immunity; autoimmunity

A

TH17

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11
Q

How are TH1 and TH17 responses similar?

A

Both driven by heterodimeric cytokines. TH1 driven by IL-12 (p35 + p40). TH2 driven by IL-23 (p19+p40).

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12
Q

What is special about IL-1

A

Very potent inflammatory cytokine. Released by caspase-1 which is activated by inflammasome.

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13
Q

Immune Deviation..

IFN-γ travels through ___ to turn on T-bet. T-bet induces ___ and TH1 response. T-bet also turns off IL-_, IL-_,IL-_.

A

Stat-1; IFN-γ; IL-4, IL-5,IL-13 and ROR-γT (TH17)

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14
Q

Immune Deviation..

IL-4 travels through ___ to turn on GATA-3. GATA-3 induces ___ and TH2 response. GATA-3 also turns off ____

A

Stat-6; IL-4 + IL-5; IFN-γ and ROR-γT (TH17)

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15
Q

TH17 response recruits what? What do they do?

A

Polymorphonuclear neutrophils (PMNs); Induce inflammation

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16
Q
Which cytokine(s)?
Inflammation; Induce TH17
A

IL-1

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17
Q
Which cytokine(s)?
Induce TH1
A

TH12

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18
Q

Typical pathogens for TH1 response?

A

Mycobacterium tuberculosis, mycobacterium leprae, Leishmania donovani

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19
Q

Where do pathogens for TH1 responses such as M. tuberculosis, M. leprae, and Leishmania donovani reside?

A

Macrophage

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20
Q

Antigen recognition site for TH1 response?

A

MHC Class II located on APC (macrophage)

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21
Q

Effector action of TH1 response?

A

Activated macrophage (via nitric oxide)

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22
Q

Typical pathogens for TH2 response?

A

Staphylococcus aureus; Streptococcus pneumoniae; Poliovirus (WHEN VIRUS INFECTS NEW CELLS AND IS THUS EXTRACELLULAR)

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23
Q

Where do pathogens for TH2 responses reside?

A

Extracellular fluid

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24
Q

Antigen recognition site for TH2 response?

A

MHC Class II located on APC (B cell)

25
Q

Effector action of TH2 response?

A

Activation of B cell to make antibody

26
Q

Roles of IFN-γ

A
  1. Induce expression of vascular adhesion molecules

2. Activate macrophages –> leads to increased release of inflammatory molecules.

27
Q

Tb Granuloma (example of inflammation induced by TH1 response to M. tuberculosis) causes what in lungs?

A

lose ability to exchange gas in alveolar sacs

28
Q

What are the two different forms of leprosy?

A

Tuberculoid leprosy; Lepromatous leprosy

29
Q

Immune Deviation…

Tuberculoid Leprosy

A

Induce appropriate TH1 response. Low infectivity. Inflammation destroys tissue and induces nerve damage –> Lose sensitivity to touch. Normal serum Ig levels.

30
Q

Lepromatous leprosy

A

Unusual form of disease. Wrong TH2 immune response. High infectivity. Can’t control bacterial growth due to wrong response. Leprosy isn’t dangerous but develop other infections.

31
Q

Which cytokines are prominent in TH1 response to tuberculosis leprosy? Lepromatous?

A

IL-2, IFN-γ, TNF-β
No IL-2, IFN-γ
Important to know that IL-4,IL5 prominent in TH2 response to Lepromatous but not tuberculoid.

32
Q

Response to parasite Leishmania?

A

TH1. Release of IFN-γ kills parasite.

33
Q

What species of in-bred mouse make a TH2 response incorrectly to Leishmania, leading to detrimental effects?

A

BALB-C; Make IL-4 instead of IFN-γ; leads to much larger lesions

34
Q

Another source of IFN-γ

A

Cytotoxic T Cells

35
Q

Example of worm infection

A

Schistosomiasis eggs induce TH2 response in the form of TH2 granulomas

36
Q

Response to worm infections?

A

TH2 response

37
Q

Presence of this lymphocyte allude to worm infection

A

Eosinophil

38
Q

What is a granuloma?

A

Collection of immune cells resulting from inflammation.

39
Q

Undifferentiated T cell path to TH1

A

Undifferentiated T cell + IL-12–> TH1 Cell via T-bet –> IFN-γ
(Defense against intracellular pathogens)

40
Q

Undifferentiated T cell path to TH2

A

Undif. T cell + IL-4 –> TH2 Cell via GATA-3 –> IL-4

defense against parasites, worms, also allergies

41
Q

Undifferentiated T cell path to TH17

A

Undif. T cell + IL-23 + IL-1–> TH17 cell via ROR-γT–> IL-17
(Defense against extracellular bacteria, autoimmunity, yeast, cancer)

42
Q

Undifferentiated T cell path to Treg

A

Undif T cell + TGF-β1–> Treg via Foxp3–> TGF-β1

(Immunosuppression) without Treg we get autoimmunity

43
Q

IL-12 induces

A

TH1 cell

44
Q

IL-4 induces

A

TH2 cell

45
Q

IL-23 and IL-1 induce

A

TH17

46
Q

Where does inducing cytokines come from?

A

APC sees TLR to induce activated APC to release IL-12

47
Q

subunits of IL-23

A

p40/p19

48
Q

subunits of IL-12

A

p40/p35

49
Q

What is IL-1 released thru?

A

caspase-1 via inflammasome activation

50
Q

What does IL-1 recruit

A

PMN to induce inflammation

51
Q

How are reactive oxygen and nitrogen species produced?

A

T cell activates macrophage

52
Q

Why do you lose nerve damage from tuberculoid leprosy

A

Quick TH1 response facilitating localized inflammation/granulomas

53
Q

T/F The wrong immune response is seen in Tuberculoid leprosy

A

F; seen in lepromatous leprosy

54
Q

IFN-gamma has what effect on macrophages infected by Leishmania?

A

macrophages kill Leishmania via cell-mediated immunity

55
Q

Why do BALB/c inbred mice exhibit large lesions from Leishmania major?

A

They make IL-4 (TH2 response) and not TL-12 (TH1)

56
Q

Schistosomiasis eggs are what type of antigen?

A

Worm–> TH2 –> Granuloma

57
Q

What is the master transcription factor for Treg

A

Foxp3

58
Q

What happens without Treg?

A

Autoimmunity