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PMCOL 344 > Immune-3 > Flashcards

Immune-3 Flashcards

1
Q

what is immunotherapy

A

any approach that manipulates the immune system of a patient for therapeutic benefit

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2
Q

what is the goal for immunotherapy

A

selectively reduce unwanted immune response but retain the other protective immune response

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3
Q

what are 2 types of effector t cells

A

CD8+ and CD4+

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4
Q

what do t regulatory cells do to CD4 cells

A

inhibits

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5
Q

what is the difference between effector t cells vs t regulatory cells with inflammation

A

effector T cells promote inflammation, regulatory T cells serve to control it

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6
Q

what are 3 examples of chronic inflammatory disorders

A
  • rheumatoid arthritis
  • multiple sclerosis
  • allergies: asthma
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7
Q

what is rheumatoid arthritis (what kind of disease)

A

multisystemic autoimmune disease

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8
Q

what is the etiopathogenesis of rheumatoid arthritis

A

unknown

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9
Q

what 2 things characterize rheumatoid arthritis

A
  • joint inflammation

- bone destruction

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10
Q

what systems does rheumatoid arthritis affect

A

joints, lung, eyes, skin, nervous system

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11
Q

what characterizes rheumatoid arthritis

A

inflammatory disease of the synovial membrane that lines surface of joints

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12
Q

what happens to the synovial membrane in rheumatoid arthritis

A

it is invaded by T and B cells and chronic inflammatory cells

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13
Q

what do osteoclases do in rheumatoid arthritis

A

osteoclasts eat the bone

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14
Q

what is the etiology and pathogenesis of rheumatoid arthritis

A

unsolved, but many genetic

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15
Q

what could be the genetic link for rheumatoid arthritis

A

MHC class 2

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16
Q

what can happen with circulating antibodies in rheumatoid arthritis

A

some have circulating autoantibodies

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17
Q

what are the autoantibodies that some rheumatoid arthritis patients have

A

rheumatoid factor (antibody) against Fc region of other antibodies

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18
Q

what happens with the synovial membrane in rheumatoid arthritis

A

it becomes infiltrated with various inflammatory cells

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19
Q

what activates T cells in rheumatoid arthritis

A

DCs

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20
Q

what do T cells stimulate in rheumatoid arthritis

A

macrophages

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21
Q

what is important for TNFalpha secretion in rheumatoid arthritis

A

T cell-macrophage contact

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22
Q

how do synovial fibroblasts and osteoclasts cause damage in rheumatoid arthritis

A

through secretion of MMPs

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23
Q

what kinds of things cause joint damage in rheumatoid arthritis

A

synovial fibroblasts, osteoclasts, cytokines

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24
Q

what stimulates B cells in rheumatoid arthritis

A

T cells

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25
Q

what are 3 things that B cells do in rheumatoid arthritis

A
  • secrete cytokines
  • act as APCs that maintain T cell activation
  • secrete antibodies
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26
Q

what kind of cascade leads to rheumatoid arthritis

A

cytokine cascade

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27
Q

what are 2 successful treatment strategies for rheumatoid arthritis

A
  • one or more disease modifying anti-rheumatic drugs (DMARDs)
  • NSAIDS or corticosteroids
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28
Q

what are DMARDs

A

agents that impede both the inflammatory and destructive processes of RA

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29
Q

what do DMARDs do

A

reduce pain and swelling and reduce the progression of destruction

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30
Q

what are 2 examples of DMARD subtypes

A

small molecule and biologics

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31
Q

what is multiple sclerosis

A

a chronic inflammatory and neurogenerative demyelinating disease of the CNS

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32
Q

when does multiple sclerosis onset usually happen

A

in young adulthood

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33
Q

what is the eiology of multiple sclerosis

A

multifactorial, involves interaction of genetic and environmental factors in a complex manner

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34
Q

what characterizes multiple sclerosis

A

autoimmune reaction against myelin

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35
Q

what kind of cells attack the myelin sheath and neurons with multiple sclerosis

A

T cells B cells and macrophages

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36
Q

what are the 3 main subtypes of multiple sclerosis

A
  • relapsing form
  • primary progressive
  • progressive relapsing
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37
Q

what % of patients have relapsing forms of MS

A

85%

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38
Q

what are the 2 types of relapsing forms of MS

A
  • relapsing remitting

- secondary progressive

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39
Q

what % of patients have primary progressive of MS

A

10%

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40
Q

what % of patients have progressive relapsing of MS

A

5%

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41
Q

what % of patients with relapsing remitting MS becomes secondary progressive MS

A

80%

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42
Q

what are 3 cell types involved in the multicellular pathophysiology of MS

A
  • infiltrating peripheral adaptive and innate immune cells

- CNS resident innate cells with inflammatory capacity

43
Q

what are the 2 CNS cells that are often involved with MS

A

Mostly astrocytes and microglia (macrophage in CNS)

44
Q

what part of the body has the first MS symptoms

A

the periphery

45
Q

what happens in the periphery in MS

A

dysregulation of immune effector-suppressor cell interactions

46
Q

what are 2 things that abnormal DC activation results in MS

A
  • increased production of pro-inflammatory cytokines

- aberrant activation of adaptive immune effectors

47
Q

what kind of cells infiltrate and damage the CNS in MS

A

autoreactive adaptive imune cells

48
Q

what kind of cells express surface molecules to penetrate the BBB in MS

A

activated immune effects (TH1 cells, CD8 cells and B cells)

49
Q

what do activated immune effects (TH1 cells, CD8 cells and B cells) do in MS

A

express surface molecules to penetrate the BBB

50
Q

what do autoreactive immune effectors and abnormally activated CNS astrocytes and microglia cause (4)

A
  • increased production of reactive species
  • excitotoxicity
  • antibody production
  • direct cytotoxicity
51
Q

where do peripheral innate and adaptive immune cells accumulate with MS

A

in perivascular space and enter the CNS parenchyma

52
Q

how do the immune cells promote demyelination

A

through direct cell contact-dependent mechanisms and through the action of soluble inflammatory and neurotoxic mediators

53
Q

what do cytokines do to t cells with MS at the BBB

A

they slow them down

54
Q

how do t cells attach to the endothelium

A

integrin/ vascular cell adhesion molecule 1 (VCAM 1)

55
Q

how do lymphocytes enter the CNS

A

via diapedesis

56
Q

what are the 3 steps for lymphocytes to enter CNS

A
  • slow down cause cytokines
  • integrin/VCAM 1: attach to endothelium
  • enter through diapedesis
57
Q

what is a late event that occurs in MS + why

A

immune cell infiltration decreases because adaptive immune cell exhaustion from chronic antigen exposure

58
Q

what 3 things continue chronic CNS instrinsic inflammation and neurogeneration

A
  • previously infiltrating adaptive immune cells
  • CNS resident innate cells
  • meningeal lymphoid like structures (SPMS)
59
Q

what do astrocytes do with late MS

A
  • produce chemokines which lead to further microglial recruitment and activation
  • inhibit progenitor cells from developing into mature ODCs
60
Q

where can clonally expanded B cells be found in late MS

A

in the meninges, parenchyma and CSF

61
Q

what is the mechanism of B cell activation, selection and maturation in MS (WHERE)

A

unclear, maybe in periphery

62
Q

what do B cells produce in MS and what is the big deal

A

produce antibodies that are detectable in CSF and are of daignostic value

63
Q

where can you detect b cell antibodies for MS

A

in the CSF

64
Q

where can antigen experienced B cells mature before transmigration into the CNS + what does this imply

A

in the cervical lymph nodes

this implies a therapeutic potential for the peripheral modulation of specific B cell subtypes

65
Q

what on the B cell in MS is a target for therapy

A

CD20

66
Q

what is immediate hypersensitivity type 1 responsible for

A

many types of allergies, like dermatitis, rhinitis, asthma, food

67
Q

what mediates immediate hypersensitivity type 1

A

IgE-FcR complex on mast cells

68
Q

what activates IgE sensitized APCs

A

allergens

69
Q

what do APCs promote with immediate hypersensitivity type 1

A

IgE production by B cells to replenish IgE consumed in the allergic reaction

70
Q

what are the 3 phases for immediate hypersensitivity type 1

A

sensitization, early and late effector phase

71
Q

what happens in the sensitization phase for immediate hypersensitivity type 1

A
  • antigen induces formation of IgE

- IgE binds by its Fc to receptors on basophils and mast cells

72
Q

what does IgE in sensitization phase for immediate hypersensitivity type 1

A

IgE binds by its Fc to receptors on basophils and mast cells

73
Q

what happens in the early effector phase for immediate hypersensitivity type 1

A
  • cross linking of cell bound IgE
  • degranulation and release of mediates
  • happens quick (mins) after reexposure
74
Q

what happens in the late effector phase for immediate hypersensitivity type 1

A
  • recruitment and activation of inflammatory cells at sites sensitive to allergens
  • peaks hours later
75
Q

how can allergens be sampled by DCs

A

in the airway lumen or through disrupted epithelium or epithelial tight cell junctions

76
Q

how can allergens enter tissues

A

through disrupted epithelium

77
Q

where does IgE bind

A

to high affinity receptor for IGE on mast cells

78
Q

where do IgE diffuse

A

locally and enters the lymphatic vessels

79
Q

what happens once IgE enters the lymphatic vessels

A

it subsequently enters the blood and is then distributed systemically

80
Q

what is a way to induce IgE production

A

TH2 activate B cells to produce it

81
Q

where do activated DCs mature and migrate to

A

regional lymph nodes or local mucosa where they activate naive T cells to TH2

82
Q

what do mast cells release once activated

A

cytokines, chemokines and growth factors

83
Q

what part of the reaction do mast cells contribute to

A

initial and the transition to late phase reaction

84
Q

what happens when the receptor recognizes the particular antigen

A

it activates mast cells to secrete preformed mediators

85
Q

what are the symptoms of the mediates

A

bronchoconstriction, vasodilation, vascular permeability, mucus production

86
Q

when does asthma occur

A

hours after allergen challenge

87
Q

what is asthma (inflammation, time line with immediate hypersensitivity type 1 )

A

late phase of inflammation, common features with early reactions

88
Q

what are 2 things involved in asthma

A
  • innate and adaptive immune cells recruited from the circulation
  • secretion of inflammatory mediators by tissue resident cells
89
Q

what causes the chronic stage of inflammation in asthma

A

repetitive of persistent exposure to allergens

90
Q

what kind of immune cells take up residence in tissues in asthma

A

innate and adaptive immune cells

91
Q

which kind of cells develop in tissue in asthma

A

more mast cells

92
Q

what is something that lots of mast cells display

A

large amounts of IgE bound to FCERI (IgE receptor)

93
Q

what is AIDS caused by

A

consequence of chronic retroviral infection with HIV

94
Q

how does AIDS virus work

A

uses host cell machinery for transcription of HIV gene products and viral replication

95
Q

what is the main thing affected in HIV

A

life threatening dysfunction of CD4+ T helper lymphocytes

96
Q

what happens to CD4 levels with AIDS

A

chronic decline, inverses CD4/CD8 ratio

97
Q

what 2 things are impaired with B lymphocytes and AIDS

A
  • marked hypergammaglobulinemia (lots of antibodies)

- impaired specific antibody responses

98
Q

what plays an important role in the pathogenesis of HIV

A

chemokines

99
Q

what determines the cell/tissue tropism of each viral strain (like macrophages, T cells

A

chemokine co receptor

100
Q

which kind of people are highly resistant to HIV

A

those with nonfunctional CCR5

101
Q

what is required for virion entry and cellular infection

A

binding to two co-receptors on targets

102
Q

what do all HIV strains express

A

gp120 that binds to CD4 molecules

103
Q

what determines the cell tropism of each viral strain

A

chemokine co receptor

104
Q

what are 2 things that are required for virion entry and cellular infection

A

CCR5 and CD4

PMCOL 344 (27 decks)

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