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MIMM 214 > Innate Immunity 5 > Flashcards

Innate Immunity 5 Flashcards

1
Q

what is the size of cytokines? is this big or small?

A

25 kD, small

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2
Q

are cytokines heterogeneous or homogeneous? what does this mean?

A

heterogeneous –> has many components so allows for many combinations with many diff functions

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3
Q

what type of molecule is a cytokine?

A

glycoprotein

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4
Q

are most cytokines soluble or membrane-bound?

A

most are soluble but some have membrane-bound forms

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5
Q

what regulates the production of cytokines?

A

post-transcription/translational modifications

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6
Q

what is the main general role of cytokines?

A

cellular communication

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7
Q

what are 3 cells that cytokines can affect? and the name for each mechanism?

A
  1. the producing cell –> autocrine
  2. adjacent cells –> paracrine
  3. distant cells –> endocrine
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8
Q

how does endocrine mechanism of cytokine activity work?

A

cytokines must go thru blood

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9
Q

what are the 4 biological functions of cytokines on target cells?

A
  1. activation
  2. proliferation
  3. differentiation
  4. survival/death
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10
Q

how do cytokines affect diapedesis?

A

change expression of adhesion molecules

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11
Q

how do cytokines affect enzymes?

A

increase/decrease activity of enzymes to change transcriptional program and change its function

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12
Q

how do cytokines affect B and T cells?

A

activate B and T cells to determine what type of cell and signal the naive T cell will get (signal 3)

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13
Q

how do cytokines cause a cytokine induction?

A

action of 1 cytokine induces that cell to produce 1 or more additional cytokines

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14
Q

what are the 5 groups of cytokines?

A
  1. interleukins (IL)
  2. interferons (IFN)
  3. tumour necrosis factors (TNF)
  4. Hematopeoitins/growth factors
  5. Chemokines
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15
Q

how many types of interleukins have been discovered so far?

A

1-37

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16
Q

what are the 3 interferons?

A

Type I:
1. IFN-alpha
2. IFN-beta

Type II:
3. IFN-gamma

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17
Q

what are the 2 types of tumour necrosis factors?

A
  1. TNF-alpha
  2. TNF-beta
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18
Q

what are 2 examples of hematopeoitins/growth factors?

A
  1. GM-CSF
  2. G-CSF
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19
Q

What are the 4 ways that cytokines can exert their effects?

A
  1. Pleiotropy
  2. Redundancy
  3. Synergy
  4. Antagonism
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20
Q

what is pleiotropy?

A

one cytokine produces many effects

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21
Q

what is redundancy?

A

more than 1 cytokine induces the same effect

22
Q

what is synergy?

A

2 or more cytokines work together to induce an effect

23
Q

what is antagonism?

A

1 cytokine can inactivate the effect of another

24
Q

describe the network of complex cytokine interactions

A

multiple cells can produce the same cytokine and each cell type can produce multiple cytokines

specific cytokines are produced at different times in different locations

25
ultimately, what determines the type of adaptive response that is produced?
cytokines
26
when does cell-mediated vs humoral immunity occur?
usually both occur, but 1 type is usually more complementary to the pathogen
27
what are 2 types of pathogens where cell-mediated immunity is favoured?
1. viruses 2. intracellular pathogens
28
what is cell-mediated immunity characterized by? (2)
1. macrophage activation 2. cytotoxic T lymphocyte activation
29
when is humoral immunity favoured?
extracellular bacteria/pathogens
30
what is humoral immunity characterized by? (2)
1. predominant B cell activation 2. predominant antibody production
31
what type of cell secretes TNF-alpha?
mainly macrophages
32
what 2 things does TNF-a stimulate?
1. migration of innate cells (diapedesis) 2. dilates blood vessels and increases clotting
33
why does TNF-a increase clotting?
to prevent pathogen from entering the bloodstream
34
what type of diseases is TNF-a involved in?
autoimmune disease --> Rheumatoid arthritis and Crohn's disease
35
why do therapies for autoimmune diseases target TNF-a?
to reduce inflammation
36
describe the effects of TNF-a in local infection (4 steps)
1. bacteria infects local tissue site 2. macrophages activated to secrete TNF-alpha in local tissue 3. increased diapedesis and blood migration at local site 4. phagocytosis
37
describe the effects of TNF-a in systemic infection (5 steps)
1. bacteria infects systemically (multiple organs) 2. macrophages in all infected organs secrete TNF-a 3. multiple areas dilate and undergo diapedesis 4. BP decreases as blood leaves so it is hard to clot blood and vessels collapse 5. multiple organ failure
38
what is sepsis?
systemic infection and inflammation
39
what induces the acute phase response?
proinflammatory cytokines
40
what are 3 proinflammatory cytokines involved in the acute phase response?
1. IL-1 2. TNF-alpha 3. IL-6
41
when does the acute phase response occur?
early on in infection
42
what occurs during acute phase response?
increased production and secretion of antimicrobial proteins from the liver, as well as other activating other processes for eliminating pathogens
43
what are 3 types of antimicrobial proteins released during the acute phase response?
1. mannose-binding lectin 2. complement components 3. C-reactive protein
44
what is the role of C-reactive protein? (2)
1. allows C1q to bind for the classical pathway in the complement system 2. opsonize bacteria
45
what are the 3 main roles of IL-1B, IL-6, TNF-a?
PRO-INFLAMMATORY against pathogen - Acute phase response - Mobilizing cells - Fever
46
what is the role of IL-1B, IL-6, TNF-a in the liver?
activate acute-phase proteins for A) activation of complement and B) opsonization
47
what is the role of IL-1B, IL-6, TNF-a in the bone marrow endothelium?
mobilize neutrophils for phagocytosis
48
what is the role of IL-1B, IL-6, TNF-a in the hypothalamus?
increased body temp for fever
49
what is the role of IL-1B, IL-6, TNF-a in fat and muscle?
protein + energy mobilization for increased body temp for fever
50
what is the role of IL-1B, IL-6, TNF-a in hypothalamus and fat+muscle? (3)
1. reduce viral and bacterial replication 2. increase antigen processing 3. increase specific immune response
51
what is the role of IL-1B, IL-6, TNF-a in dendritic cells?
TNF-a stimulates migration to lymph nodes + dendritic cell maturation to initiate adaptive immune response
52
why does fever/increased body temp kill pathogen? (2)
1. pathogens need 37degC so anything high is bad 2. possible evidence that high temp increases efficiency of immune cells

MIMM 214 (33 decks)

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