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Zach- Immunology > Lecture 4-1 > Flashcards

Lecture 4-1 Flashcards

1
Q

What are neutrophils?

A

-circulating effector cells that are active in early phagocytosis of microbes

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2
Q

What are macrophages?

A
  • circulating effector cells of innate immunity

- phagocytosis and killing of microbes

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3
Q

What are NK cells?

A

-circulating effector cells of innate immunity that lyse infected cells and activate macrophages

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4
Q

What is C-reactive protein?

A
  • pentraxin
  • circulating effector protein
  • opsonizes microbes, activates complement cascade
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5
Q

What is mannose-binding lectin (collectin)

A
  • circulating effector protein

- opsonize microbes and activates the lectin complement cascade

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6
Q

What is the complement protein?

A
  • circulating effector protein

- activates leukocytes, kills microbes, opsonizes microbes

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7
Q

What type of response do cytokines TNF, IL-a, and chemokines generate?

A

inflammatory

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8
Q

What type of response is generated by IFN-alpha/Beta?

A

resistance to viral infection

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9
Q

What response is activated by IFN-gamma?

A

macrophage activation

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10
Q

What type of response does IL-12 generate?

A

stimulates IFN-gamma production and NK and T cells

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11
Q

What type of response does IL-15 generate?

A
  • proliferation of NK cells
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12
Q

What type of response does IL-10 and TGF-beta stimulate?

A
  • helps to control inflammation
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13
Q

What is a PAMP? pathogen associated molecular pattern

A
  • specific motif in non-self Ag that allow the innate immune system to recognize them as threats
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14
Q

What are PRRs? pathogen recognition receptors

A

-PRRs are responsible for recognizing the PAMPs which are specific to gram (+)(-)

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15
Q

What feature do prokaryotes contain that is unique to them and allows the PMN cells to bind to?

A

N-formylmethionyl peptide is present and allows the PMN cells to bind and initiate phagocytosis

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16
Q

Which TLR (toll-like receptors) are located intracellularly, within an endosome?

A

TLR-3,-7,-8,-9

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17
Q

What pathogen does TLR-3 recognize?

A

dsRNA

  • carried on NK cells
  • located in endosomes
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18
Q

What pathogen does TLR-7 recognize?

A

ssRNA

  • at endosome
  • carried by plasmacytoid DC, NK, B cell, eosinophils
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19
Q

What pathogen does TLR-8 recognize?

A

ssRNA

  • at endosome
  • carried by NK cells
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20
Q

What pathogen does TLR-9 recognize?

A

CpG DNA

  • at endosome
  • carried by B cells, eosinophils, basophils, plasmacytoid DC
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21
Q

What TLR are located extracellularly?

A

TLR- 1,2,4,5,6

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22
Q

TLR-1,-2 heterodimer responds to what pathogen?

A
  • lipopeptides, GPI
  • at PM
  • carried on monocytes, DC, basophils, mast cells
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23
Q

TLR-2 responds to what pathogen?

A

bacterial peptidoglycan

24
Q

TLR-4 homodimer responds to what pathogen?

A

Lipopolysaccharides

  • at PM
  • carried on macrophages, DC, mast cells, eosinophils
25
Q

TLR-5 responds to what pathogen?

A

bacterial flagellin

  • at PM
  • on cells in the intestinal epithelium
26
Q

TLR-2,-6 heterodimer responds to what pathogen?

A
  • lipoteichoic acid, zymosan
  • at PM
  • carried on monocytes, DC, basophils, mast cells
27
Q

What is the overall product of activating a TLR?

A

-leads to large activation of NF-kappaB

which is a pro-inflammatory protein

28
Q

What TLR use MyD88 in order to activate NF-kappaB and interferon response factors (IRF)?

A

-1,-2,-5,-6,-4,-7,-9

29
Q

Which TLR use TRIF in order to activate interferon response factor (IRF) and NF-kappaB?

A

-4,-3

30
Q

What does activation of the TLR lead to?

A
  • antimicrobial pathway to kill pathogen directly
  • induce tissue apoptosis to the host cells
  • cause septic shock
  • mostly will activate NF-kappaB which produces inflammatory genes
31
Q

Describe the cascade pathway after a TLR is activated and how the NF-kappaB initiates the production of pro-inflammatory genes.

A
  • the kinase cascade activates IKK by phosphorylation
  • IKK binds with NF-kB and allows degradation of inhibitory protein IkB.
  • active NF-kB enters the nucleus, activates transcription, and inflammatory genes are synthesized and secreted va the ER
32
Q

What signaling molecules are largely released by necrotic tissue?

A

DAMPs, damage associated molecular patterns

33
Q

What are common DAMPS? damage associated molecular patterns?

A
  1. HMGB1
  2. Uric acid
  3. HSPs
34
Q

What does the release of HMGB1 indicate, what does it cause, and where does it bind?

A
  1. indicates necrotic tissue
  2. activates the NF-kB pathway
  3. Bind to the RAGE receptor on DC
35
Q

What does the release of uric acid indicate, what does it cause, and where does it bind?

A
  1. indicates necrotic tissue
  2. activates the NF-kB pathway
  3. this has an unknown receptor on DC
36
Q

What does the release of HSP indicate, what does it cause and where does it bind?

A
  1. indicates necrotic tissue
  2. induces the NF-kB pathway, release of TNF-alpha and IL-1B, inflammatory genes
  3. binds to CD91 on DC
37
Q

What are NLRs used primarily for in the host?

Nucleotide oligomerization domain like receptors

A
  1. specialized gorup of intracellular proteins
  2. regulate the host innate immune response
  3. activate NF-kB and mitogen activated protein kinase pathways
38
Q

Overall the NLR (nucleotide oligomerization domain like receptors) have what function?

A
  1. regulate the host innate immune response by activating the inflammatory caspases
39
Q

What is an inflamasome?

A
  1. signaling complex of NLR and other proteins that form in response to PAMPs and DAMPs
40
Q

What enzyme do inflammasomes activate?

A

caspase-1

41
Q

What is the function of caspase-1?

A
  • cleave inactive cytoplasmic precursor form of IL-1B and IL-18.
  • the cleavage leads to activation of these cytokines and produces and inflammatory response
42
Q

What response do IL-1B and IL-18 produce?

A
  • pro-inflammatory response
43
Q

What are the different type of receptors that contribute to form the scavenger receptor (SR) family?

A
  1. scavenger receptor class A type I
  2. scavenger receptor class A type II
  3. MARCO
44
Q

What are the three distinct domains on the SRs?

A
  1. Cysteine rich domain (absent on TypeII)
  2. collagen like domain
  3. alpha-helical coiled coil system (absent in MARCO)
45
Q

What is the primary purpose of SRs?

A
  • uptake of oxidized lipoproteins

- also bind and uptake bacterial cells with negative charges

46
Q

Which SRs are expressed on tissue macrohpages and help with recognition of microorganisms?

A

SR-B and CD 36 whose main function is to eliminate the microbe

47
Q

TLR-2,-6 has uses a coreceptor to recognize lipoteichoic acid and diacylated lipopeptides. what is that coreceptor?

A

CD36

48
Q

What type of bacterial components are SR most likely to bind to?

A
  • negatively charged components

- lipoteichoic acids, nucleic acids, B-glucan, proteins, LPS

49
Q

What is the primary function of lectin receptors?

A
  • facilitate phagocytosis of microbes
  • secrete cytokines to promote adaptive immune response
  • contain carbohydrate recognition domain
50
Q

What will recognize 1) terminal D-mannose, 2) L-fucose, 3) N-acetyl-D-glucosamine sugar?

A

mannose receptors which is a C-type lectin

51
Q

What do defensins do to microbes?

A

-infiltrate and disrupt the function of the microbial membrane

52
Q

Defensins are activated by what process and are largely located in what area?

A
  • located in epithelial cells, neutrophils, NK cells, CTLs, (cytotoxic T lymphocyte) granule containing leukocytes
  • stimulated by cytokines and microbial products
53
Q

What are antimicrobial peptides largely produced by neutrophils?

A
  • cathelicidins
54
Q

What effect do cathelicidins have when released?

A
  • toxic to microorganisms
  • activate leukocytes
  • anti-inflammatory role by blocking inflammasome activation
55
Q

What are two ways that antimicrobial peptides (cethelicidins) can be activated?

A
  1. stimulus from microbe

2. PMN can release antimicrobial peptides in resposne to cytokines

56
Q

What multiple processes can AMPs produce when released beneath the epidermis?

A
  1. promote angiogenesis
  2. wound repair
  3. activate TLR-9
  4. recruit T cells
  5. degrade mast cell, histamine release–>vasodilation
  6. block TLR activation
  7. neutralize proinflammatory gene release from monocytes/macrophages

Zach- Immunology (10 decks)

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