Innate Immunity 4 Flashcards

1
Q

can receptors be homodimers or heterodimers?

A

both

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2
Q

how do receptors dimerize?

A

by ligands aka the pathogen

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3
Q

what are 2 types of receptors that are heterodimers?

A

TLR2 and TLR4

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4
Q

what is the only molecule that results from PRR?

A

cytokines

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5
Q

what are 5 cytokines that cause inflammation?

A
  1. IL-1
  2. IL-6
  3. IL-8
  4. TNF-alpha
  5. IL-12
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6
Q

what are 2 cytokines that cause antiviral effects?

A
  1. IFN-alpha
  2. IFN-beta
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7
Q

what does IFN stand for?

A

interferon

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8
Q

what are 2 types of chemokines?

A
  1. CC chemokines
  2. CXC chemokines
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9
Q

what is different about CC and CXC chemokines?

A

different location of the 2 cysteine residues

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10
Q

what are 3 effects of PRR signaling?

A
  1. cytokine production
  2. increased expression of costimulatory molecules
  3. enhanced migration to regional/secondary lymphoid
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11
Q

what are 2 costimulatory molecules produced by PRR signaling?

A
  1. B7.1/CD80
  2. B7.2/CD86
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12
Q

what do B7.1/CD80 and B7.2/CD86 do?

A

provide SIGNAL 2 to T cells in lymphoid tissues

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13
Q

where are costimulatory molecules located?

A

on dendritic cells

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14
Q

why are costimulatory molecules located on dendritic cells?

A

because they need to present to lymphoid tissue

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15
Q

how does PRR signaling cause enhanced migration to regional, secondary lymphoid organs?

A

upregulates specific adhesion molecules

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16
Q

what is the result of migration to regional, secondary lymphoid lymphoid organs?

A

T cells activate

17
Q

what are the steps of Type I IFN signaling?

A
  1. IFN secreted upon PRR signaling
  2. IFN binds to receptors on surrounding cells
  3. triggers signaling in nucleus
  4. transcription of genes that inhibit viral replication
  5. halt/slow virus infection
18
Q

what type of molecules causes migration of dendritic cells?

A

costimulatory molecules

19
Q

what happens if transcription factors for IFN cannot reach nucleus?

A

everything in cytoplasm works normally to produce the transcription factor, but it remains in the cytoplasm and cannot activate IFN genes

20
Q

what is the term for migration of neutrophils and phagocytes to the site of inflammation?

A

chemotaxis

21
Q

what type of cells do adhesion molecules recruit?

A

monocytes

22
Q

describe how monocytes move to site of infection by adhesion molecules?

A

adhesion molecules line the endothelium and bind the monocyte

when the monocyte receives the chemokine signal, the monocyte migrates into the surrounding tissue and differentiates into an inflammatory monocyte at the site of infection

23
Q

what are the 3 types of adhesion molecules?

A
  1. selectins
  2. integrins
  3. immunoglobulin superfamily
24
Q

are all adhesion molecules throughout the body?

A

different types of adhesion molecules in different tissues

25
Q

how do leukocytes move thru the body?

A

adhesion molecules WEAKLY bind the leukocyte so the cell can roll across the endothelium thru the bloodstream

26
Q

what are 4 symptoms that result from the recruitment of leukocytes?

A
  1. heat
  2. redness
  3. swelling
  4. pain
27
Q

why does icing help with inflammation? and why should you not ice for too long?

A

reduces vasodilation but don’t ice for too long bc could prevent immune cells from functioning

28
Q

what is diapedesis?

A

when cell crosses from the lumen of a vessel btwn endothelial cells into surrounding tissues

29
Q

what are the 4. steps of cell migration?

A
  1. rolling adhesion along endothelial cells
  2. tight binding at adhesion molecules, held in one place
  3. diapedesis (migration into tissue)
  4. migration towards high [chemokines] where pathogen is
30
Q

when are more adhesion molecules expressed at the endothelium?

A

when cytokines/chemokines are released, they bind endothelium to cause more adhesion molecule expression

31
Q

what happens to the blood vessel upon migration?

A

vasodilation

32
Q

when does arthritis/loss of function occur?

A

with severe/chronic inflammation