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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
Q

ultimately, what determines the type of adaptive response that is produced?

A

cytokines

26
Q

when does cell-mediated vs humoral immunity occur?

A

usually both occur, but 1 type is usually more complementary to the pathogen

27
Q

what are 2 types of pathogens where cell-mediated immunity is favoured?

A
  1. viruses
  2. intracellular pathogens
28
Q

what is cell-mediated immunity characterized by? (2)

A
  1. macrophage activation
  2. cytotoxic T lymphocyte activation
29
Q

when is humoral immunity favoured?

A

extracellular bacteria/pathogens

30
Q

what is humoral immunity characterized by? (2)

A
  1. predominant B cell activation
  2. predominant antibody production
31
Q

what type of cell secretes TNF-alpha?

A

mainly macrophages

32
Q

what 2 things does TNF-a stimulate?

A
  1. migration of innate cells (diapedesis)
  2. dilates blood vessels and increases clotting
33
Q

why does TNF-a increase clotting?

A

to prevent pathogen from entering the bloodstream

34
Q

what type of diseases is TNF-a involved in?

A

autoimmune disease –> Rheumatoid arthritis and Crohn’s disease

35
Q

why do therapies for autoimmune diseases target TNF-a?

A

to reduce inflammation

36
Q

describe the effects of TNF-a in local infection (4 steps)

A
  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
Q

describe the effects of TNF-a in systemic infection (5 steps)

A
  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
Q

what is sepsis?

A

systemic infection and inflammation

39
Q

what induces the acute phase response?

A

proinflammatory cytokines

40
Q

what are 3 proinflammatory cytokines involved in the acute phase response?

A
  1. IL-1
  2. TNF-alpha
  3. IL-6
41
Q

when does the acute phase response occur?

A

early on in infection

42
Q

what occurs during acute phase response?

A

increased production and secretion of antimicrobial proteins from the liver, as well as other activating other processes for eliminating pathogens

43
Q

what are 3 types of antimicrobial proteins released during the acute phase response?

A
  1. mannose-binding lectin
  2. complement components
  3. C-reactive protein
44
Q

what is the role of C-reactive protein? (2)

A
  1. allows C1q to bind for the classical pathway in the complement system
  2. opsonize bacteria
45
Q

what are the 3 main roles of IL-1B, IL-6, TNF-a?

A

PRO-INFLAMMATORY against pathogen
- Acute phase response
- Mobilizing cells
- Fever

46
Q

what is the role of IL-1B, IL-6, TNF-a in the liver?

A

activate acute-phase proteins for A) activation of complement and B) opsonization

47
Q

what is the role of IL-1B, IL-6, TNF-a in the bone marrow endothelium?

A

mobilize neutrophils for phagocytosis

48
Q

what is the role of IL-1B, IL-6, TNF-a in the hypothalamus?

A

increased body temp for fever

49
Q

what is the role of IL-1B, IL-6, TNF-a in fat and muscle?

A

protein + energy mobilization for increased body temp for fever

50
Q

what is the role of IL-1B, IL-6, TNF-a in hypothalamus and fat+muscle? (3)

A
  1. reduce viral and bacterial replication
  2. increase antigen processing
  3. increase specific immune response
51
Q

what is the role of IL-1B, IL-6, TNF-a in dendritic cells?

A

TNF-a stimulates migration to lymph nodes + dendritic cell maturation to initiate adaptive immune response

52
Q

why does fever/increased body temp kill pathogen? (2)

A
  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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