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HDM > Final > Flashcards

Final Flashcards

1
Q

Do you normally find cytokines in the blood stream? What kind of signaling are they?

A

no- only find in blood in sick people

act locally in a paracrine or autocrine fashion

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2
Q

After binding to their receptors, what do cytokines produce?

A

changes in pattern of RNA and protein synthesis

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3
Q

What two types of pathways do cytokines utilize?

A

JAK-STAT or Ras-MAP kinase pathways

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4
Q

Describe the pathway of JAK-Stat pathway

A

cytokines bind receptors which are bound to JAKs
conformational change activates Jaks->trans/auto-phosphorylation of the two bound Jaks
Jaks phosphorylate cytokine receptors
Stat proteins by receptor chains
Jaks phosphorylate Stats
Stats from dimer and translocate to nucleus

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5
Q

what are the five critical roles of cytokines?

A
  • inflammatory reactions (pro and anti)
  • linking innate and adaptive immunity
  • activation of T cells (Th1/Th2 polarization)
  • activation of B cells and Ab production (isotype switching)
  • important for control of hematopoiesis (leukocytosis)
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6
Q

What does we mean when we say cytokines are pleiotropic??

A

exhibit multiple effects on growth and differentiation of a variety of cell types

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7
Q

What is an example of cytokines being redundant?

A

activated Th cells produce IL-2,4,5 to cause proliferation of B cells

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8
Q

What is an example of synergy in cytokines?

A

Th cells produce both IL-4 and IL-5 to induce a class switch to IgE in B cells

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9
Q

What is an example of antagonism in cytokines?

A

activated Th cells produce both IL-4 and IFN-y which work against each other. IFN-y blocks class switching to IgE induced by IL-4

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10
Q

What does a cytokine cascade look like?

A

one cytokine induces production of another

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11
Q

What are the 8 cytokines that promote acute inflammatory?

A

TNF-a, IL-1, IL-6, IL-8, IL-11, IL-12, IL-15, IL-18

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12
Q

What type of transcription do pro-inflammatory cytokines have?

A

NF-kB-dependent transcription

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13
Q

What are the two main anti-inflammatory cytokines?

A

IL-10 and TGF-B

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14
Q

What type of transcription do anti-inflammatory cytokines have?

A

NF-kB-indepdent transcription

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15
Q

If the body is overwhelmed by inflammatory cytokines what occurs?

A

systemic inflammation -> severe sepsis -> cardiovascular collapse and multiple organ failure

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16
Q

What are the first things macrophages will produce when activated and in what order?

A

TNF, IL-1, IL-6

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17
Q

If someone has a genetic abnormality in the synthesis of active TNF, what happens? Why?

A

they’ll be more sensitive to a lower concentration of bacteria
there is a couple hours of delay before IL-1 and IL-6 are produced and that’s enough time for bacteria to reproduce

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18
Q

Which is a more powerful inducer of inflammation: IL-1 or TNF?

A

TNF

we need less of it compared to IL-1

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19
Q

What are ways of reducing biological activities of TNF and IL-1?

A

neutralizing antibodies, soluble receptors, receptor antagonists

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20
Q

What do TNF or IL-1 produce when administered to humans?

A

fever, systemic inflammation, shock, and death

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21
Q

In what patients has blocking TNF and IL-1 been highly successful?

A

patients with rheumatoid arthritis, inflammatory bowel disease, GVHD

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22
Q

What patients is blocking TNF and IL-1 not successful? Why?

A

patients with sepsis

by the time the patient presents to you they are beyond the stage of just TNF and IL-1

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23
Q

What are systemic effects of TNF/IL-1?

A 
fever
leukocytosis
increase in APPs
decrease in appetite
increase in sleep
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24
Q

What are local effects of TNF/IL-1 on vascular endothelium?

A

increase in expression of leukocyte adhesion molecules
production of IL-1, chemokine
increase procoagulant and decrease anticoagulant activity

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25
Q

What cells produce TNF-B? What cells produce TNF-a?

A

macrophages and monocytes —> TNF-a
T lymphocytes —> TNF-B
neutrophils, NK cells

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26
Q

What is the most potent inducer of TNF?

A

endotoxin: LPS

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27
Q

What occurs when TNF interacts with endothelial cells/

A

induces ICAM-1, VCAM-1, and E-selectin to permit the egress of granulocytes into inflammatory loci

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28
Q

What is the primary mediator for septic shock?

A

TNF

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29
Q

What is a potent activator of neutrophils? What does it mediate?

A

TNF

adherence, chemotaxis, degranulation, and respiratory burst

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30
Q

What are the TNF receptors?

A

TNF receptor I (TNFR p75) and TNF receptor II (TNFR p55)

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31
Q

How does TNF affect cancerous cells?

A

induces antitumor immunity through direct cytotoxic (apoptotic) effects

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32
Q

What are the primary producers of IL-1? What else produces IL-1?

A

primary: macrophages and monocytes

neutrophils, endothelial cells, keratinocytes

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33
Q

What is IL-1 the first in line to do?

A

interact with CNS to produce fever

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34
Q

What effects does IL-1 produce?

A

fever, lethargy, sleep

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35
Q

What cytokine produces anorexia?

A

TNF

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36
Q

What is IL-1 second in line to TNF to do?

A

stimulate ICAM-1, VCAM-1, and E-selectin on endothelial cells and neutrophils

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37
Q

What is the only cytokine to induce production of IL-2? In what cells?

A

IL-1 induces production of IL-2 by and proliferation of CD4 T lymphocytes

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38
Q

So what cytokine is only produced by innate immune cells?

A

IL-1

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39
Q

What is IL-1 second in line to IL-6 to do?

A

stimulate synthesis of APPs

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40
Q

What can IL-1 be neutralized by?

A

natural IL-1 receptor antagonist IL-1ra

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41
Q

What is IL-6 primarily produced by? But also by?

A

primarily: mononuclear phagocytic cells

T and B lymphocytes, fibroblasts, endothelial cells, keratinocytes, hepatocytes, bone marrow cells

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42
Q

What is IL-6 the most important inducer of?

A

APP

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43
Q

What stimulates differentiation of B lymphocytes into mature plasma cells?

A

IL-6

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44
Q

What has a primary role in TH17 immune regulation?

A

IL-6

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45
Q

What primarily produces IL-8? What releases IL-8 on the onset of inflammation?

A

primarily macrophages

mast cells

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46
Q

What is IL-8 a chemotactic factor for?

A

neutrophils but not monocytes!

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47
Q

What cytokine controls cell-mediated immunity? How?

A

IL-12 by activation of Th1 T cells

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48
Q

What does IL-12 stimulate and activate?

A

stimulates IFN-y production

activates and induces proliferation, cytotoxicity, and cytokine production of NK cells

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49
Q

What does IL-12 synergize with? To do what?

A

synergizes with IL-18 (aka IFN-y-inducing factor) to stimulate IFN-y release

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50
Q

What primarily produces IL-15?

A

mononuclear phagocytic cells

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51
Q

What is the most important activity of IL-15?

A

activation of NK cells

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52
Q

What type of growth factor is IL-15?

A

T cell growth factor

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53
Q

What is IL-15 a chemotactic factor for?

A

T lymphocytes

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54
Q

What interleukin is important for the survival of CD8 memory T cells?

A

IL-15

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55
Q

What cells primarily make IFN-y?

A

Th1 T cells and NK cells

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56
Q

What is the most important cytokine for cell-mediated immunity?

A

IFN-y

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57
Q

How does IFN-y take care of killing intracellular bacteria?

A

stimulates phagocytosis, secretion, respiratory bursts, and NO production in tissue macrophages

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58
Q

Who induces synthesis of IFN-y in Th cells and NK cells?

A

IL-18

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59
Q

What all does IFN-y stimulate?

A
  • killing by NK cells and neutrophils
  • expression of MHC class I and II
  • Ag presentation by APCs
  • cytokine production by APCs
  • expression of ICAM-1
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60
Q

What does IFN-y inhibit?

A

allergic responses by suppressing many IL-4-mediated effects

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61
Q

What cytokine has modest antiviral activity?

A

IFN-y

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62
Q

What antagonist is a major anti-inflammatory cytokine?

A

IL-1 receptor antagonist (IL-1ra)

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63
Q

What cells primarily produce IL-10?

A

macrophages, B cells, Treg cells

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64
Q

What does IL-10 inhibit?

A

production of IL-1B, IL-6, IL-8, IL-12, TNF-a by mononuclear phagocytes
expression of class II MHC by APCs
expression of CD80/CD86 by APCs
production of IFN-y and TNF-B by TH1 lymphocytes
production of IL-4and IL-5 by Th2 lymphocytes

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65
Q

What cytokine controls tolerance to environmental allergens?

A

IL-10

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66
Q

What is the most pleiotropic of the cytokines? Why?

A

TGF-B

has both stimulatory and inhibitory effects on numerous cell types

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67
Q

Who primarily produces TGF-B?

A

macrophages and Treg cells

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68
Q

What does TGF-B stimulate?

A

fibrosis promoting wound healing and scar formation

apoptosis in B cells and CD8 T lymphocytes

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69
Q

What does TGF-B inhibit?

A
  • proliferation of B cells and CD8 T lymphocytes

- macrophages and NK cells

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70
Q

What cytokine regulates the differentiation of Th17 lymphocytes?

A

TGF-B

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71
Q

What type of response causes asthma? Tuberculosis?

A

asthma is Th2

Tuberculosis is Th1

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72
Q

What are the cytokines of the adaptive immunity?

A

IL-2, IL-4, IL-5, IL-17
IFN-y
TGF-B

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73
Q

What cytokine stimulates Th cells differentiating into Th1 cells? What is their transcription factor?

A

IFN-y

T-bet

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74
Q

What cytokine stimulates the differentiation of Th cells into Th2 cells? What is their transcription factor?

A

IL-4, IL-5, IL-13

GATA-3

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75
Q

What cytokine stimulates the differentiation of Th cells into Th17 cells? What is their transcription factor?

A

IL-17A, IL-17F, IL-22

RORyT

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76
Q

What type of Th cell is big in alternative macrophage activation?

A

Th2 cells

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77
Q

What will Th1, Th2, and Th17 express?

A

CD4+ since they’re all differentiated Th cell

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78
Q

What cells will proliferate if exposed to IL-2? Why only these cells?

A

activated T cells (have antigens)

naive T cells have low affinity IL-2 receptors

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79
Q

What does IL-2 increase the expression of on activated T cells?

A

IL-2R

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80
Q

When the Ag is cleared, what happens to the IL-2R? Who blocks IL-2 induced proliferation to control T cells?

A

IL-2R numbers decline

TGF-B blocks IL-2-induced proliferation

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81
Q

What interleukin induces differentiation of a Th0 cell into a Th1 cell?

A

IL-12

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82
Q

What do Th1 cells secrete? What do they promote?

A

IL-2, IFN-y, TNF-B

cell-mediated immunity

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83
Q

What cytokine induces differentiation into a Th2 cell?

A

IL-4

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84
Q

What do Th2 cells activate?

A

B lymphocytes

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85
Q

What does IFN-y inhibit when it comes to T cells? What about IL-10/IL-4?

A

Th2 cell proliferation

Th1 cell proliferation

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86
Q

What two other cells do Th1 cells support?

A

produce IFN-y to activate phagocytes to kill

stimulate the production of antibodies which promote the phagocytosis of microbes

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87
Q

How will mice that are infected with M. tuberculosis (intracellular) react if they are (IFN-y+, IL-12+)?

A

they can control infection and will survive

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88
Q

How will mice that are IL-12 knockout mice (IFN-y+) react to infection with M. tuberculosis?

A

they cannot control infection and die because no TH1-type of adaptive immunity is developing in mice

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89
Q

How will IFN-y KO mice (IL-12+) react to infection with M. tuberculosis?

A

die early because macrophages are not activated properly in the absence of IFN-y

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90
Q

What is the association between Th2 cells and IgE antibody?

A

Th2 cells produce IL-4 which stimulate the production of IgE antibody

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91
Q

what is IgE’s role in host defense?

A

participates in the activation of mast cell by protein antigen
binds to helminths

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92
Q

What activates eosinophils? What cells produce it?

A

IL-5 from Th2 cells

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93
Q

What cytokine induces the isotype switch to IgG?

A

IFN-y

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94
Q

What cytokines induce the isotype switch to IgA? Where is it produced?

A

TGF-B, BAFF produced in mucosal tissues

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95
Q

What cytokine induces the isotype switch to IgE?

A

IL-4

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96
Q

What receptors do growth factors bind to?

What kind of receptor is this?

A

Type I cytokine receptors

Jak-STAT

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97
Q

What receptors do interferons bind to?

A

type II cytokine receptors

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98
Q

What receptors do TNF-a and B bind to?

A

TNF receptor family

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99
Q

What receptors do IL-1 and IL-18 bind to?

A

IL-1 receptor family

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100
Q

What receptors do IL-10 bind to?

A

Type II cytokine receptor

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101
Q

What cells express the enzyme 5-LO?

A

macrophages, mast cells, basophils, neutrophils

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102
Q

What cells can be induced to express 5-LO?

A

monocytes

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103
Q

What is the function of 5-lipoxygenase?

A

AA —> leukotriene (LTA4)

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104
Q

What is 5-LO’s accessory protein?

A

5-LO activating protein (FLAP)

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105
Q

Are leukotrienes hormones?

A

no they’re autocoids!

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106
Q

What is the receptor for LTA4?

A

There is none, it’s a biosynthetic intermediate

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107
Q

What leukotrienes control bronchoconstriction and mucus secretion? What are their receptors?

A

LTC4 and LTD4

CysLT1 and CysLT2

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108
Q

What leukotriene is in charge of neutrophil chemotaxis and degranulation? What is its receptor?

A

LTLB4

BLT1,2

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109
Q

Pyogenic infection have pus that is rich in what?

A

neutrophils!

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110
Q

Why will people who are complement deficient still have neutrophils showing up at infection sites?

A

5-LO is working and will produce LTB4

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111
Q

What is another function of the inflammation mediators produced by phagocytes and granulocytes?

A

tells epithelial and mesenchymal cells in the area to adapt, migrate or perish
to limit damage that is inevitable with inflammation

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112
Q

What cells are in charge of the inflammatory reaction in asthma? What mediators do they produce?

A

Th2
IL-4, -5, -13
TNF-a
LTB4

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113
Q

What does the initial exposure to an allergen generate and what is this called?

A

IgE antibodies

sensitization

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114
Q

What does a subsequent exposure to an allergen cause in IgEs?

A

cross links the IgE receptors

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115
Q

What does cross-linking IgE receptors trigger?

A

degranulation (release of histamine)

activation of eicosanoid biosynthesis (LTC4, LTD4, PGD2)

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116
Q

How does histamine effect the capillaries?

A

increases permeability of the capillaries to other leukocytes and plasma proteins

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117
Q

When IgE recognizes an antibody, what does the mast cell it’s attached to do?

A

degranulates- releases histamine

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118
Q

What does it mean when we say histamine is pre-formed? Where is it pre-formed?

A

synthesized and stored

in granules of mast cells and basophils

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119
Q

What is an example of a substance that complexes with histamine to keep it inactive?

A

heparin

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120
Q

What receptor does histamine have to bind to to cause vasodilation and increased permeability?

A

H1 receptors

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121
Q

Why is there pain at sites of infection?

A

histamine binds to H1 receptors on peripheral nerves

and mechanical pressure of tissue swelling on nerves

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122
Q

What does binding of histamine to H2 receptors cause?

A

increased gastric acid secretion in stomach

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123
Q

What tissues express both H1 and H2 receptors?

A

heart, blood vessels, skin capillary blood vessels

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124
Q

Where do we find mast cells?

A

nasal passage, trachea, bronchi, lungs, stomach, intestines, skin

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125
Q

What does IL1B induces expression of?

A

adhesion molecules on endothelium

COX-2 in macrophages, monocytes, connective tissue and endothelium

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126
Q

What engulfs uric acid crystals and triggers IL1B and IL8 release?

A

macrophage/monocytes

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127
Q

What eicosanoid causes vasodilation?

A

PGI2

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128
Q

What eicosanoid causes permeability?

A

PGE2

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129
Q

Leaky vessels allow plasma extravasation into interstitial space and causes what?

A

localized edema

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130
Q

What is the most sensitive techniques for labeling?

A

radioactivity

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131
Q

Why isn’t radioactivity used more?

A

presents health hazards

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132
Q

What kind of labeling is currently most used in labs?

A

fluorescence labels

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133
Q

What protein used in fluorescence labels is re from cyanobacteria?

A

PE (phycoethrin)

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134
Q

What molecule provides a green light for fluorescence labels?

A

FITC (fluorescein isothiocyanate)

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135
Q

What is the main technique for detecting presence of antigen in tissue?

A

indirect immunostaining

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136
Q

A reaction between Ag-Ab may lead to precipitation and is the basis for what lab technique?

A

agglutination

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137
Q

What does formation of Ag-Ab complexes lead to? How do we observe this?

A

increase in light scattering

observed with naked eye or photometrically using turbidimetric or nephelopmetric detection

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138
Q

What is the requirement for agglutination?

A

have to have multiple sites for interaction on both Ag or Ab

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139
Q

The more Ag-Ab complexes formed the more transparent or less transparent the liquid will be?

A

less transparent

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140
Q

A polyvalent Ag is a molecule with multiple? What is it capable of?

A

epitopes

can react with several Ab molecules

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141
Q

As cross linking between polyvalent Ags occurs what will happen?

A

become less stable —> agglutination

eventually complex will precipitate

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142
Q

What pH is ideal for the maximum specific agglutination? What happens if the pH is less than idea?

A

neutral pH

below 6 proteins will self-agglutinate

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143
Q

A polyclonal antiserum is usually used for?

A

immunoagglutination

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144
Q

A direct agglutination assay has high potential for an error when there is an excess of what?

A

Ag

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145
Q

In indirect agglutination assay, why do we measure with an excess of antigen?

A

Test antigen will displace manufacturer made complexes

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146
Q

What do you measure in indirect agglutination assay?

A

measuring for displacement of manufacturer made complexes

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147
Q

Ouchterlony immunodiffusion involves the migration of Ab and Ag towards each other in? What will you see?

A

semisolid agar gel

a visual precipitate is formed

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148
Q

Where will a visual precipitate form in ouchterlony immunodiffusion?

A

where the concentrations of Ab and Ag become equivalent

149
Q

How do you set up a plate for Ouchterlony immunodiffusion?

A

antiserum (Abs) placed in center well

each Ag in surrounding wells

150
Q

What are three characteristic precipitation reactions that can occur in Ouchterlony analysis?

A

identity
non-identity
partial identity

151
Q

What technique is used for rapid Ag quantification in complex samples?

A

immunoelectrophoresis

152
Q

What is the result of the immunoelectrophoresis and what is it proportional to?

A

each sample gives a “rocket”

length of which is proportional to the concentration of Ag in sample

153
Q

What is used to identify monoclonal immunoglobulins (M-component) associated with myeloma (plasma cell neoplasia)?

A

immunoelectrophoresis

154
Q

How are M-components identified? How do we detect this?

A

abnormal band in the gamma-globulin region (occasionally in the beta)
IEP

155
Q

How is the resolution of IEP improved? What chemical do we use?

A

staining

Coomasssie Blue R-250

156
Q

What technique is used for ABO blood grouping?

A

hemagglutination (Coombs) assay

157
Q

What does Coombs assay detect?

A

RBC Ags or Abs present in the sample against RBC Ags

158
Q

What technique can be observed and used to make diagnosis with just the naked eye?

A

coombs assay

ABO blood grouping

159
Q

What is used to detect Rh in mother and fetal blood?

A

indirect coombs assay

160
Q

All leukocytes express what CD?

A

CD45

161
Q

All T cells express

A

CD3

162
Q

All B cells express

A

CD19

163
Q

What technique uses a particular cell type to identify, count, separate out cells from a mixture of different cells?

A

fluorescence-activated cell sorting (FACS)

164
Q

Treg cells express

A

CD25

165
Q

sIgA (secreted IgA) and sIgM limit the colonization by pathogens. What is this called?

A

immune exclusion

166
Q

If food proteins and microbiota suppress Th2, Th1 and Th17 responses what is this called?

A

oral tolerance

167
Q

Production of what pro-inflammatory mediators can cause hyper immunity?

A

IL-6, IL-12, TNF

168
Q

Mutations in what immune-regulatory proteins can cause immunodeficiency?

A

NOD2 or IL-10

169
Q

In the absence of commensal Bacteroides, what binds to TLR5 on intestinal cells and activates NF-kB via IKK?

A

salmonella flagellin

170
Q

What exports activated NF-kB from the nucleus and is associated with Bacteroides?

A

peroxisome proliferator-activated receptor (PPAR)

171
Q

Where is a chronic immune-inflammatory response NOT triggered?

A

mucosa

172
Q

What type of cells is tolerance of microflora related to?

A

tissue macrophages

dont sense microflora and thus do not secrete cytokines

173
Q

What pathway does commensal microflora suppress?

A

NF-kB

174
Q

What is it called when genetic factors and environmental factors result in disruption of the microflora?

A

dysbiosis

175
Q

What does dysbiosis result in?

A

loss of protective bacteria and accumulation of pathobionts

176
Q

What does an accumulation of pathobionts and loss of protective bacteria result a hyper activation of?

A

Th1 and Th17 cells

177
Q

Commensal bacteria tend to have anti-inflammatory activities. They induce what/

A

Greg cells, IL-10, and REGIIIy

178
Q

What is an islet-derived anti-microbial protein that is induced by commensal bacteria?

A

REGIIIy

179
Q

Segmented filamentous bacteria (SFB) induce the expansion of what cells?

A

Th17 cells (pro-inflammatory)

180
Q

If a patient has chronic inflammation due to opportunist pathogens in the gut, what should you suspect to be wrong?

A

reduced immune responses

181
Q

If the levels of regulation and pro inflammatory stimuli are basal, yet there is colitis (inflammation) what should you suspect?

A

enhanced immune reactivity

182
Q

What happens to expose the immune system to a great amount of pro inflammatory stimuli which can overcome intestinal regulation?

A

disruption of the intestinal barrier

183
Q

The normal reaction of the immune system to intestinal stimuli can result in chronic inflammation if there’s an absence of what?

A

Treg cells

184
Q

What occurs when the intestinal regulatory mechanisms outweighs inflammatory signals induced by the immune system reacting to the stimuli from the flora?

A

GI immune homeostasis

185
Q

Prevention of inflammation may be achieved through regulation of what?

A

epigenetic

186
Q

What controls the balance between tolerance and pro inflammatory responses and are also essential for immunological development?

A

environmental signals

187
Q

What is markedly decreased in germ-free mice?

A

IgA-producing cells and Th17 cells

188
Q

What promotes intestinal barrier function and helps to maintain host-commensal mutualism?

A

SIgA

189
Q

How does SIgA maintain host-commensal mutualism?

A

coats commensal and pathogenic bacteria to inhibit their binding to the host epithelium and their penetration of the lamina propria

190
Q

Expression of what CD is found in Treg cells?

A

FOXP3

191
Q

Why does depletion of Treg cells result in intestinal inflammation?

A

expansion of CD4+ Th cells specific to commensal bacteria

192
Q

What type of bacteria promote the generation of Th17 cells in mice/

A

segmented filamentous bacteria (SFB)

193
Q

What cytokines do Th17cells produce that play a role in autoimmune disease?

A

IL-17 and IL-22

194
Q

What cells do Treg cells suppress?

A

Th1, Th2, Th17

195
Q

The gut lamina prpria contains a lot of what?

A

J-chain expressing IgA and IgM

196
Q

How doe endothelial cells exert a local gatekeeper function for mucosal immunity?

A

they direct migration of B and T cells by expression adhesion molecules and chemokines

197
Q

Activation of T cells in intestinal immunity occurs where?

A

in the MLNs (mesenteric lymph nodes)

198
Q

How do antigens recognized by intestinal immune system?

A

enters through M cells and transfers to local DCs

or enters through epithelium covering the villus

199
Q

What cells in the intestines can express MHC II and act as local APCs?

A

enterocytes

200
Q

Where do blood antigens interact with T cells?

A

peripheral lymph nodes

201
Q

what cells overlie payer’s patches and lymphoid follicles to facilitate luminal sampling?

A

M cells

202
Q

What do M cells exhibit that allows them to promote uptake and transport of luminal contents?

A

reduced mucin secretion and modified apical and basolateral surfaces

203
Q

What cells can extend up between tight junctions of intestinal epithelial cells to sample luminal contents?

A

dendritic cells

204
Q

Where do professional APCs reside in the Peyer’s patches and lymphoid follicles?

A

subepithlial dome (SED)

205
Q

What are the two general functions of neutrophils?

A

granulocytes and phagocytes

206
Q

How can inflammation aggravate gout?

A

uric acid precipitates more easily at acid pH

207
Q

What causes systemic inflammation throughout the vasculature?

A

LPS (bacteria) and cytokines (TNFa)

208
Q

What causes the drop in blood pressure which is a feature of septic shock?

A

systemic vasodilation and extravasation of plasma from blood to interstitial space

209
Q

In anaphylaxis, what do we see happen due to histamine?

A

drop in blood pressure
increase in blood vessel permeability
increase in peripheral edema

210
Q

What compounds the effects of histamine in allergy and anaphylaxis?

A

autocoid lipid mediators such as LTC4, LTD4, PGD2

211
Q

What type of receptors cause bronchoconstriction when stimulated?

A

PGD2 and DP receptors

212
Q

What are three major areas of diversity related to the mechanisms of immunogenetics?

A

immunoglobulins, T cell receptors, MHC

213
Q

Will each antibody produced by a plasma cell respond to different antigens?

A

NO they all respond to a specific antigens

214
Q

If a single plasma cell secretes a bunch of immunoglobulins (different isotopes) what will they respond to?

A

the same antigen!

215
Q

What are the two light chain isotypes and can they be mixed on the same immunoglobulin?

A

kappa or lambda

NO they have to have two of either of them

216
Q

What isytopes have three constant domains in the heavy chain?

A

d, y, a

217
Q

What isotypes have four constant domains?

A

u and E

218
Q

Expression of an Ig heavy chain involves what two gene recombination events?

A

D-J joining

Joining of V region to DJ complex

219
Q

In Ig light chains and the TCR a chain, a V gene recombines with what?

A

directly with a J gene segment

220
Q

In what things do you find a D region?

A

Ig heavy chain

TCR B chain

221
Q

What’s the difference between kappa and lambda light chain genes?

A

kappa- 1 constant region

lambda- 4 constant regions

222
Q

What type of diversity is almost unlimited due to the removal of nucleotides from V, D, and J segments by exonuclease at time of recombination? What enzyme helps?

A

junctional diversity

terminal deoxyribonucleotidyl transferase (TdT)

223
Q

What diversity is limited by number of available V, D, and J gene segments and involves V(D)J recombinase?

A

combinational diversity

224
Q

What is the dos important site for antigen recognition on a TCR?

A

CDR3

225
Q

in isotype switching, what is deleted?

A

DNA (This rarely happens in other cells)

226
Q

B cells can accumulate point mutations in the DNA encoding their VL or HL regions. These mutations may increase the affinity of the antibody tot he epitope. what is this called?

A

affinity maturation

227
Q

What are the principle determinants for graft acceptance or rejection between individuals?

A

MHC proteins (HLA)

228
Q

Peptides in the cytosol are associated with? What are they recognized by?

A

MHC I

CD8+ T cells

229
Q

Peptides in vesicles are associated with? What recognizes them?

A

MHC II

CD4+ T cells

230
Q

What are the three polymorphic genes of MHC II?

A

HLA- DR, -DQ, -DP

231
Q

Which class has more diversity: MHC I or II?

A

II because a and B chains are polymorphic

232
Q

What do CD 8+ T cells bind to on MHC class I?

A

a3- it does not vary

233
Q

What do CD4+ T cells bind to on MHC class II?

A

B2 domain

234
Q

Grafts where tissue is moved from on place to another on the same individual are called?

A

autografts

235
Q

Transplants between genetically identical individuals are called?

A

isografts

236
Q

Grafts between genetically different members of the same species are called? What’s an example?

A

allogenic grafts

kidney transplants

237
Q

Grafts between members of different species are called? What’s an example?

A

xenogeneic grafts

pig heart valves to humans

238
Q

HLA typing for tissue transplants typically focuses on?

A

HLA-A, -B, -DR

239
Q

What four things do you check for tissue transplants?

A

ABO blood typing
HLA typing
screening for preformed antibodies
crossmatching

240
Q

What causes apoptosis in cancer cells?

A

TNF

241
Q

What is a major activator of intracellular killing of pathogens by tissue macrophages?

A

IL-18

242
Q

What inhibits allergic responses by suppressing many IL-4 mediated effects?

A

IFN-y

243
Q

What inhibits expression of class II MHC by APCs?

A

IL-10

244
Q

What transcriptional factor is unique for T reg cells?

A

FOXP3

245
Q

What induces a Th0 cell to become a Th17 cell?

A

IL-1, IL-6

246
Q

What blocks IL-2-induced proliferation which is a key mechanism for control of T cells proliferation?

A

TGF-B

247
Q

What induces a Th cell to become a Th2 cell?

A

IL-4

248
Q

What inhibits Th2 cell proliferation?

A

IFN-y

249
Q

What inhibits Th1 cell proliferation?

A

IL-10, IL-4

250
Q

After naive T cells have been activated by DCs, pathogen-specific T cells are made by?

A

clonal expansion

251
Q

Loaded DCs move in to the T cell zone located in the?

A

parafollicular cortex

252
Q

Autoimmunity results from a breakdown of what?

A

self-tolerance

253
Q

The induced apoptosis of T lymphocytes that react too strongly to self-Ags is called what?

A

negative selection

254
Q

What type of tolerance is induced in immune self-reactive lymphocytes in generative lymphoid organs?

A

central tolerance

255
Q

What type of tolerance is induced in mature self-reactive lymphocytes in peripheral sites?

A

peripheral tolerance

256
Q

What ensures that mature lymphocytes are NOT reactive to self-aga but it’s not always perfect?

A

central tolerance

257
Q

What prevents activation of potentially dangerous lymphocytes (self-reactive)?

A

peripheral tolerance

258
Q

If a TCR has no affinity for self peptide what happens in the thymus?

A

cell undergoes spontaneous apoptosis because it does not receive survival signal

259
Q

If TCRs have a high affinity for self peptide what happens in the thymus?

A

receive death signal and undergo apoptosis

260
Q

Mutations in what gene results in failure of central tolerance?

A

AIRE

261
Q

What disease results from a mutation in AIRE? How would these patients present?

A

autoimmune polyendocrine syndrome (APS)

destruction of endocrine organs by antibodies, lymphocytes

262
Q

What is AIRE’s role in the thymus?

A

it’s a transcription factor that is associated with expression of self-Ags by thymic epithelial cells

263
Q

What regulates the expression of tissue-restricted Ags?

A

AIRE

264
Q

In the absence of fictional AIRE, what are not eliminated?

A

self-reactive T cells

265
Q

What is another function of T cells that have a strong recognition of Self Ags?

A

they become Treg cells that enter peripheral tissues

266
Q

Why are Treg cells not eliminated by apoptosis even though they recognize self-Ags?

A

they produce anti-apoptotic molecules which protects them from negative selection

267
Q

What does some generation of Treg cells require?

A

TGF-B

268
Q

What do Treg cells express high levels of that other T cells express normal levels of?

A

CTLA-4- inhibitory analog for CD28

269
Q

What interleukin does the survival and functional competence of Treg cells depend on?

A

IL-2 and FOXP3

270
Q

Expression of what makes Treg cells regulatory cells?

A

FOXP3

271
Q

With an increase in differentiation there is a decrease in what in cells?

A

proliferative ability

272
Q

What cytokine induces a Th0 cell to become a Treg cell?

A

TGFB

273
Q

What are two ways you can get Treg cells?

A

natural Treg cells are generated in thymus

inducible Treg cells are produced by Ag recognition in LNs

274
Q

What stimulates production of IgA by inducing B cells to switch?

A

TGF-B

275
Q

If there is a FoxP3 deficiency, what is their impaired production of? What is this syndrome called?

A

Reg cells

IPEX syndrome

276
Q

What is an intrinsic signal for apoptosis?

A

Cyt C, Granzyme

277
Q

Defective development, survival or function of Treg cells an cause inflammatory bowel disease, anti-erythrocyte and anti-DNA autoantibodies. What must be mutated?

A

IL-2 or IL-2Ra/B

278
Q

There is a failure of anergy in CD4+ T cells leading to lymphoproliferation, T cell infiltrates in organs especially the heart, and patient is dead with 3-4 weeks. What must be mutated?

A

CTLA-4

279
Q

When T cells recognize self Ags they may use a receptor whose function is to terminate T cell responses. What would this receptor be?

A

CTLA-4

280
Q

What is expressed on Treg cells and mediates the suppressive function of these cells by inhibiting the activation of naive T cells?

A

CTLA-4

281
Q

T cells enter a tumor microenvironment and they’re induced to overexposes CTLA-4 so they cannot induce cell cycle arrest in tumor cells. What would you treat these patients with?

A

antibodies directed against CTLA-4

282
Q

What would antibodies against CTLA-4 result in?

A

T cell activation which gives you a strong response against tumor cells

283
Q

What has a higher affinity for CD 80/86 than CD28?

A

CTLA-4

284
Q

So if you have a patient who is experiencing autoimmunity, what is one way to block it?

A

give them soluble CTLA-4

285
Q

If a B cell responds to a self Ags with high avidity what happens to it?

A

either apoptosis or it edits the specificity of its BCR

286
Q

If a B cell has a weak recognition of self Ags in the bone marrow what happens to it?

A

anergy of the B cells

287
Q

In B cells, CD22 recruits what enzyme to attenuate B cell receptor signaling?

A

SHP-1 tyrosine phosphatase

288
Q

What is the process called that results from t cells being physically separated from their specific Ag and therefore cannot become activated?

A

immunologic ignorance

289
Q

The process known as deletion causes T cells to undergo apoptosis due to a signal they receive from APCs. What is this signal?

A

FasL

290
Q

What is the CD for Fas?

A

CD95

291
Q

What is the CD for CTLA4?

A

CD152

292
Q

Suppression of other cells by Treg cells is due to a release of what cytokines?

A

IL-10 and TGFB

293
Q

How can genetics confer susceptibility to autoimmunity?

A

influencing maintenance of self-tolerance

294
Q

What has to happen to induce autoimmunity?

A

an environmental trigger such as infection or other inflammatory stimuli

295
Q

What type of immunity usually dominates autoimmunity?

A

adaptive immunity

296
Q

What genes have the strongest association with autoimmunity?

A

MHC genes

297
Q

What type of infection is rheumatic fever triggered by? It’s mediated by a cross-reactivity between these bacteria Ags and what?

A

streptococcal infection

cardiac myosin

298
Q

In multiple sclerosis, T cells react with what protein from what viruses?

A

myelin basic protein

Epstein-Barr virus, influenza virus type A, human papillomavirus

299
Q

What is an example of polyclonal activation?

A

LPS activating B cells via TLR4

300
Q

What is it called when a microbial infection causes activation of bystander auto reactive lymphocytes via a cytokine field?

A

polyclonal activation

301
Q

When microbes kill cells what can be released? What can be a result of this?

A

sequestered Ags

inflammation and autoimmunity

302
Q

What exacerbates lupus in mouse models by altering B-cell repertoire in the absence of inflammation?

A

estrogens

303
Q

What’s an example of a reason why autoimmune diseases being more common in women than in men?

A

estrogens alter B-cell repertoire in the absence of inflammation

304
Q

What drugs can bind to RBC membrane and generate a neoantigen that elects an auto-Ag that causes hemolytic anemia?

A

penicillins and cephalosporins

305
Q

The blockade of what can induce antinuclear Abs and even lupus and multiple sclerosis?

A

TNF-a

mechanism is unknown

306
Q

What are three examples of noninfectious triggers of autoimmunity?

A
  • estrogens
  • drugs (penicillins and cephalosporins)
  • blockade of TNF-a
307
Q

What types of hypersensitivity are antibody-mediated?

A

Type I, II, III

308
Q

What types of hypersensitivity are cell-mediated?

A

Type IV

309
Q

Type I hypersensitivity results from the actions of mediators secreted by what?

A

mast cells

310
Q

In type II hypersensitivity, antibodies are made against what?

A

tissue Ags

311
Q

In type III hypersensitivity, Abs bind what? Where are these complexes deposited?

A

circulating Ags

deposit in vessels causing vasculitis

312
Q

What cells cause the inflammation of type IV hypersensitivity? What cells kill host cells?

A

Th1 and Th17 cells

CD8+ CTLs

313
Q

What antibody dominates type I hypersensitivity?

A

IgE

314
Q

If an individual has a strong propensity to developing allergic reactions they are said to be?

A

atopic

315
Q

In type I hypersensitivity, IgE Abs are produced against what type of antigens?

A

environmental

316
Q

IgE Abs bind to what on the membrane of mast cells and basophils? Does it have low or high affinity?

A

FcER1

high affinity

317
Q

When there is initial contact with an allergen, what does IgE do?

A

becomes fixed on the surface of mast cells or basophils

318
Q

When there is second contact with an allergen, where does the reaction predominantly occur?

A

Ag-Ab reactions occur predominantly on the mast cell and basophil membrane

319
Q

Why does repeatedly exposing a patient to higher concentrations of an allergen usually get rid of an allergic response?

A

they start producing IgG which will compete with IgE at low concentrations of the allergen

320
Q

What interleukin is big in type I hypersensitivity and what cells produce it?

A

IL-4

Th2 cells

321
Q

How long after a first exposure to an allergen will it take to get an allergic reaction to the allergen again?

A

5-7 days

322
Q

What are characteristics of the immediate phase of type I hypersensitivity?

A

vascular and smooth muscle reaction: vasodilation, congestion, edema

323
Q

What are characteristics of the late phase of type I hypersensitivity? How long until this reaction develops?

A

inflammatory infiltrate rich in eosinophils, neutrophils, T cells
2-24 hours later

324
Q

What causes dilation of small blood vessels and increased vascular permeability in type I hypersensitivity?

A

histamine

325
Q

What causes damage to local tissues in type I hypersensitivity?

A

proteases

326
Q

What causes vascular dilation in type I hypersensitivity?

A

prostaglandins

327
Q

What stimulates prolonged smooth muscle contraction in type I hypersensitivity?

A

leukotrienes

328
Q

What induces the late-phase reaction (inflammation) of type I hypersensitivity?What’s an example? By what pathway?

A

cytokines- TNF

NF-kB

329
Q

What is the minimum number of receptors that must be engaged to get a strong response in type I hypersensitivity?

A

two!

330
Q

What are the effectors for anaphylaxis? Antigens?

A

IgE on basophils and mast cells

insect venom, drugs, food

331
Q

What are the effectors of asthma and hay fever?

A

IgE on mast cells and Th2 cells

332
Q

What are the effectors of food allergies?

A

IgE on mast cell and Th2 cells

333
Q

How can differentiate anaphylaxis from asthma?

A

vascular collapse and death occurs with anaphylaxis

334
Q

What antibodies are involved in type II hypersensitivity?

A

IgG and IgM

335
Q

How do IgG antibodies produce and pro inflammatory response?

A

bind to neutrophil and macrophage Fc receptors and activate them

336
Q

What causes damage in adjacent tissues in type II hypersensitivity?

A

reactive oxygen species and lysosomal enzymes that are released from neutrophils and macrophages

337
Q

Autoimmune hemolytic anemia is what type of hypersensitivity? What’s the mechanism?

A

type II

opsonization and phagocytosis of erythrocytes due to Rh blood group antigens

338
Q

Rheumatic fever is an example of what type of hypersensitivity?

A

type II

339
Q

Vascular inflammation is a result of what type of hypersensitivity?

A

type III

340
Q

What is the major mechanism triggering tissue damage in type III hypersensitivity?

A

classical activation of complement

341
Q

What causes serum sickness?

A

IV administration of anti-serum

342
Q

What is the reaction that is induced by subQ administration of a protein Ag to a previously immunized animal?

A

arthus reaction

343
Q

What reaction results in the formation of immune complexes at the site of Ag injection and local vasculitis?

A

arthus reaction

344
Q

Systemic lupus erythematous is what type of hypersensitivity?

A

type III

345
Q

What are the major causes of T cell-mediated hypersensitivity reactions?

A

autoimmunity and exaggerated responses to environmental Ag

346
Q

What are the mechanisms of tissue injury for type IV hypersensitivity?

A

Th1 and Th17 cells producing cytokines —> inflammation

killing of host cells by CD8+ CTLs

347
Q

Delayed type hypersensitivity is caused by activated?

A

Th1 cells

348
Q

Can only extracellular pathogens cause sensitization phase of DTH?

A

nope intracellular also can

349
Q

Upon re-encounter with Ag, Th1 clones undergo further clonal expansion and secrete what that activates macrophages?

A

IFNy and TNF-B

350
Q

What hypersensitivity requires the transfer of antigen-specific Th1 clones to be passively transferred?

A

type IV

351
Q

How can type I, II, III reactions be transferred?

A

by serum containing Abs

352
Q

What are examples of type IV hypersensitivities?

A

type 1 diabetes, MS, rheumatoid arthritis

353
Q

What is tissue injury a result of in type IV hypersensitivity?

A

products of the recruited and activated neutrophils and macrophages such as lysosomal enzymes, ROS, NO, and pro inflammatory cytokines

354
Q

The inflammation associated with T cell-mediated diseases is typically…

A

chronic

355
Q

How long does delayed type hypersensitivity usually take to develop?

A

24-48 hours after Ag challenge

356
Q

TB, poison ivy, and diptheria/tetanus toxins are all things that can sensitize humans for what?

A

DTH reactions

357
Q

Purified protein derivative (PPD) is an antigen of what? and what type of reaction does it elicit?

A

mycobacterium tuberculosis

elicits a DTH reaction aka tuberculin reaction

358
Q

How do corticosteroids work?

A

block NF-kB

359
Q

What would inhibitors of calineurin, Jaks and other kinases do?

A

inhibit signaling!

immunotherapy

360
Q

What would an anti-IL-2R immunotherapy do?

A

block T cell proliferation

361
Q

What would an anti-IL-17 immunotherapy do?

A

block inflammation

362
Q

What would an anti-p40 immunotherapy do?

A

block Th1, Th17 responses

363
Q

What would anti-integrins immunotherapy do?

A

block adhesion

364
Q

What would anti-TNF, anti-IL-1, and anti-IL-6R immunotherapy do?

A

block inflammation obvi

365
Q

What would anti-CD40L immunotherapy do?

A

inhibit cell-cell interaction and leukocyte migration

366
Q

What would anti-CD20 Ab immunotherapy do?

A

depletion of cells and antibodies specifically B cells

367
Q

How do regulatory T cell-based therapies work?

A

expand and activate Treg cells in culture and transfer them back to the patients

368
Q

What makes a B cell very sensitive to antigens?

A

CR2

369
Q

What is a requirement for T helper cell to be involved in activation of B cell?

A

presentation of peptide Ag wishing class II MHC

HDM (3 decks)

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