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Host Defense > T cell Robinson > Flashcards

T cell Robinson Flashcards

1
Q

Gamma Delta T cells

A

MHC type system that recognizes lipid rich antigens

  • important for host/environment interfaces
  • produce several early cytokines like 1, 6
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2
Q

Gamma Delta T cells

A

MHC type system that recognizes lipid rich antigens

-important for host/environment interfaces

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3
Q

What are T cells responses regulated by?

A

specific cytokines and Tregs

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4
Q

What type of antigen conformations do antibodies recognize?

A

3D

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5
Q

What type of antigen conformations do t-cells recognize?

A

peptides in the context of MHC

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6
Q

If an antigen is prestented by an MHC2 to a niave CD4 Tcell what 4 responses could occur?

A

Th1, Th2, Th17, Treg

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7
Q

If an antigen is presented by an MHC2 to a naive CD4 T Cell what 4 responses could occur?

A

Th1, Th2, Th17, Treg

-commitment to a subset depends on host genetics, type of infection, and which type of TLR and cytokine profile

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8
Q

Th1

A

enhances and amplifies cellular mediated immunity by activating macrophages/ and or promoting cytotoxic responses by CD8

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9
Q

Th2

A

promotes optimal antibody production

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10
Q

Th17

A

chronic inflammation

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11
Q

Treg

A

modulates or suppresses immune responses

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12
Q

T-FH

A

high affinity antibody production in the germinal center of a lymph node

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13
Q

What does commitment to a subset depend on?

A

which TLR system is activated and which cytokine profile becomes dominant at the time of presentation

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14
Q

Where do activation steps of the various cd4 cells occur?

A

following initiation-activation steps occur in the secondary lymphoid tissues

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15
Q

How many chain peptides are on a cytokine?

A

2 usually encoded by separate genes

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16
Q

What 2 things do all cytokines exhibit?

A

pleiotropism and redundancy

-at concentrations similar to hormones

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17
Q

What do lymphocytes and macrophages use cytokines for?

A

to regulate the intensity of an immune response

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18
Q

Do most cell/cytokine systems have agonist/antagonist dynamics?

A

yes

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19
Q

Can cytokines actions vary and depend on the state of the target cell?

A

yes

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20
Q

What provokes the classic Th1 response?

A

Infections by organisms that require phagocytosis and intracellular killing

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21
Q

What is the obligatory Th1 helper initiator cytokine?

A

12

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22
Q

What is the obligatory Th1 helper initiator cytokine?

A

12(also has a potent effect on NK cells)

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23
Q

What co-stimulatory molecules do Th1 cells upregulate when activated?

A

CD 28 and CD 154 (40L)

REQUIRED DETERMINANT

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24
Q

What cytokines does Th1 provide to propagate the TMMI response?

A

IL-2 and INF gamma

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25
Q

What 3 things is INF gamma produced by?

A
  1. Th1(CD4)
  2. NK
  3. activated CD8 cells
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26
Q

What 3 things does INF gamma do?

A
  • activator of macrophages
  • upregulated of MHC2 and endothelial receptors
  • suppressor of Th2 and Th17
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27
Q

What does Il21 do and what produces it, what 2 circumstances does it exist?

A

Th1 cells produce IL 21-
potent promoter of CD8 killing acitivity

in absence of INF gamma it is a potent promoter of B cell growth and development

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28
Q

What is IL 2 produced by?

A

Th1 and CD8

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29
Q

What strongly depends on IL2?

A

Tregs

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30
Q

What does IL 2 do?

A
  • critical growth cytokine
  • acts in autocrine and paracrine needs
  • IL2R expressed as a functional unit after antigen activation
  • genetic defects in its assembly result in severe immune deficiency disease
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31
Q

What has Th1 helper activation developed to provide?

A

an antigen specific way to recruit highly activated macrophages

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32
Q

Can small numbers of Th1 recruit vast numbers of macrophages?

A

yes

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33
Q

The end result of TMMi is activated macrophage, what does the macrophage produce? What do these cytokines do?

A

-Tetrad
1, 6, 8, and TNF alpha

-wide range of autocrine and paracrine and systemic effects that promote inflammation

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34
Q

What does pro-inflammatory IL 1 respond to? What 4 functions does it have?

A

-responds to stress

  1. promotes neutrophil growth and emigration from the marrow
  2. Acts with IL 6 on CNS to cause fever, depression
  3. neuroendocrine effects on adrenal gland
    * 4. Stimulates APCs to increase Ag presentation

-antagonist is IL-1Ra

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35
Q

What does pro-inflammatory IL 1 respond to? What 4 functions does it have?

A

-responds to stress

  1. promotes neutrophil growth and emigration from the marrow
  2. Acts with IL 6 on CNS to cause fever, depression
  3. neuroendocrine effects on adrenal gland
    * **4. Stimulates APCs to increase Ag presentation

-antagonist is IL-1Ra

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36
Q

What does IL6 a pro-inflammatory cytokine do?

A
  • many effects redundant with Il-1
    1. primary cause of fever and other constitutional signs of infection
    2. T-cell “vitamin” it promotes responsiveness to IL-2, accelerates antigen activation
  • **3. strong growth and differentiation effects on Bcells in the presence of other B cell cytokines and effects on bone mineral metabolism where it activates osteoclasts
  • it is required for optimal Th17 development
  • may be required for Th-FH development
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37
Q

WHat does TNF alpha a proinflammatory cytokine do?

A
  • Plays a central role in the immune system
    1. macrophage activator
    2. activator of endothelial homing and adhesion molecules
    3. upregulates MHC and other cytokines
    4. potent inducer of apoptosis and angiogenesis
  • systemic effects that range from flu-like symptoms to death
  • positive feedback
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38
Q

WHat does TNF alpha a proinflammatory cytokine do?

A
  • **Plays a central role in the immune system
    1. macrophage activator
    2. activator of endothelial homing and adhesion molecules
    3. upregulates MHC and other cytokines
    4. potent inducer of apoptosis and angiogenesis
  • systemic effects that range from flu-like symptoms to death
  • **positive feedback
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39
Q

What does IL 8 do? When is 8 produced?

A
  • *1. NEUTROPHILS to the site of infection
  • produced mainly by macs, neutrophils, and during intense inflammation by endothelial cells
  • actually a chemokine
40
Q

What does delayed hypersensitivity mean?

A

archaic term for TMMI

41
Q

What is the bump from TB skin testing from?

A

macrophages recruited by CD4

42
Q

What is the bump from TB skin testing from?

A

macrophages recruited by CD4

-less than 5% will be TB specific T cells

43
Q

What is an example of non specific lymphocyte cytotoxicity?

A

Natural Killer Cells

  • *no Ag receptors
  • older than T cells
  • are not MHC restricted
44
Q

What do Natural killer cells produce?

A

INF gamma

45
Q

How do natural killer cells kill?

A
  1. **killing mechanism suppressed by normal MHC-1
    - ->activated by altered MHC-1 in combination with activating ligand on the target cell
  2. when pathogen complexed with antibody, natural killer cells through their Fc receptors recognize target cell with antibodies and kill it
46
Q

What is an example of antigen specific cytotoxicity?

A

CD8

  • recognize and kill foreign, mutated and viral infected cells
  • recognition is via display of endogenously produced antigen in MHC-1 determinant
47
Q

What do Natural killer cells produce?

A

INF gamma, IL21, IL2

48
Q

When is there optimal activation of CD8?

A
  1. NK cells
  2. CD4 helper cells
  3. memory cells
49
Q

What do Natural killer cells produce?

A

INF gamma, IL21, IL2 (antigen activated CD4 continues to produce these)

50
Q

What 2 things does CD8 need to be activated?

A
  1. correct MH1 with specific antigen

2. INF gamma (produced by NK and CD4)

51
Q

Do CD8 cells require co-stimulatory signal?

A

No, can kill repeatedly

52
Q

What turns CD8 cytotxicity off?

A

dependent on viral display on targets, in the absence of specific targets they activate their own death by gnes Fas/FasL
-10% become memory cells

53
Q

What turns CD8 cytotoxicity off?

A

dependent on viral display on targets, in the absence of specific targets they activate their own death by genes Fas/FasL
-10% become memory cells

54
Q

What does the a dominant IL-4 cytokine cause?

A

Th2

55
Q

Do Th1 and Th2 occur at the same time?

A

NO

56
Q

What do B-cells recognize?

A

extracellular or soluble antigens

57
Q

What are the cells that drive T0-T2?

A
  • committed Th2 cells
  • B cell presentation of antigen
  • Mast Cells
  • DC and TLR under specific gene influences
58
Q

What is required for Th2 and what is that requirements major source?

A

Il4

major source Th2

59
Q

What 3 cytokines are the major drivers of B cell differentiation and isotype switch?

A

IL 5,6, 10

-major source of these is TH2 cell

60
Q

What 3 cytokines are the major supressors of a Th1 reaction?

A

Il 4, 10, 13

13 is a critical player in IgE

61
Q

What 3 cytokines are the major suppressors of a Th1 reaction?

A

Il 4, 10, 13

13 is a critical player in IgE

62
Q

What are the functions of Th2 response?

A

-Enhance b cell function and ultimately antibody produciton

  • makes pathogens more attractive to macs and polys
  • bind toxins
  • target mutant/viral infected cells for killing
63
Q

What is the costimulatory signal for the Th2 B cell response?

A

CD 40/ 40L

64
Q

What is the dominant T helper response dictated by?

A

the type of infection, the type of TLR activated and the dominant cytokines present

65
Q

What type of things invaders a Th 17 response?

A

Bacteria and Fungi that live outside of host cell

66
Q

What do bacteria and fungi trigger?

A

DCs to produce TGF beta, IL6, and IL 17

67
Q

What does Th17 produce?

A

IL 17

68
Q

What does IL 17 do?

A

recruits neutrophils

69
Q

Which ILs have to do with neutrophils?

A

8 ,7

70
Q

Which ILs have to do with neutrophils?

A

8, 17

71
Q

What does IL 17 do?

A

recruits neutrophils

-an inflammatory cytokine

72
Q

Does Th17 have a central role in autoimmune disease?

A

yes

73
Q

What are the cell surface markers on CD4 Th1 Regs?

A

3, 4, 25+ and Fox P3+

74
Q

What are CD4 Th1 Regs influenced by and what do they depend on?

A

TGF beta

-depend on IL2 for survival

75
Q

T follicular helper cells do?

A
  • restricted to B-cell follicles in lymphoid tissue
  • promotes high affinity antigen specific B cell response
  • CD278, IL6, IL21
76
Q

How does B-cell capture an antigen in the extracellular environment?

A

by displaying its specific angtigen receptor on its cell surface

77
Q

What is Th17 suppressed by?

A

Th1 and Th2 and T regulator cells

78
Q

When are iTregs induced?

A

during a normal immune response as a break mechanism on proliferation

79
Q

What happens to stimulated T cells that do not receive co-stimulatory signals CD80 (b-7)

A

inactivation
convert to tregs
or commit suicide

80
Q

That is the transcriptional factor of Tregs?

A

Fox P2

CD3, 4, 25+

81
Q

That are key features of Tregs?

A

Fox P2
CD3, 4, 25+
and express CTLA4

82
Q

What does CTLA4 do?

A

supresses T-call activation by competing with CD28 and down regulating CD80(B7) on DC

83
Q

What is CTLA4 expression controlled by?

A

FoxP3

84
Q

What is CTLA4 expression controlled by?

A

FoxP3

-someone gets sick and someone doesnt its cause CTLA-4 is highly polymorphic

85
Q

Where can Tregs arise?

A

thymus
regional lymph nodes
peripheral sites (especially the gut)

86
Q

What are converted to T-regs at peripheral sites during ongoing immune reactions when local cytokine concentrations begin trending to TGF-B and LESS IL6?

A

Tho–>Tregs

87
Q

What happens as TGF-B becomes dominant?

A
  • FoxP3 upregulated CTLA-4

- shuts down APC

88
Q

Can Tregs make IL2?

A

NO but are dependent on it for IL2 survival and function

89
Q

WHat strategies does the immune system ivoke to combat viral infections?

A

ALL STRATEGIES

90
Q

Why is a b-cell response necessary in a viral infection?

A

Because the infection can leave the infected cell and that when B cells get it

91
Q

What are CD8 memory cells called?

A

CD8-RM(resident memory)

92
Q

How do CD8RM cells work?

A

Restrict their traffic patterns to areas of past infections and this enables them to rapidly respond to repeat infection

93
Q

What happens to CD4-RMs when an antigen is not present?

A

they disappear

-when antigen is present they form clusters with macrophages

94
Q

What do memory cells produce?

A

Il2, Il 21, and INF gamma that concomitantly activate an innate antiviral response

95
Q

What is a side benefit to Memory cells/?

A

they prime the area of residence to be hyperreactive to viruses and presumable bacterial that were not the initial pathogens
-probably by training the macrophages by epigenetic mechanisms

Host Defense (11 decks)

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