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SFM Quiz 2 > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

What is sebum?

A

Substance made of lactic acid and fatty acids that reduce the skin pH to between 3-5. This inhibits the growth of microbes.

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2
Q

What sentinel cells detect pathogens and begin the inflammatory response?

A

Mast cells, macrophages, and dendritic cells

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3
Q

What are pathogen-associated molecular patterns (PAMPs) and what are their key properties?

A

They are effective indicators of the presence of a particular pathogen. They (1) are unique to particular classes of pathogens, (2) cannot be altered, suppressed, or hidden, (3) have no structural similarity with self antigens.

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4
Q

How is the mannose receptor PAMP specific for pathogens?

A

Because it targets glycans with a terminal mannose, which is not found in humans.

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5
Q

List the Toll-Like Receptors (TLRs) that recognize extracellular pathogens and intracellular pathogens.

A

Extracellular: TLR-1, -2, -4, -5, -6
Intracellular: TLR-3, -7, -8, -9

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6
Q

What are the ligands/microorganisms recognized by TLR1:TLR2 heterodimer?

A

Lipopeptides/Bacteria and GPI/Parasites

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7
Q

What are the ligands and microorganisms recognized by TLR2:TLR6 heterodimer?

A

Lipoteichoic acid/Gram-positive bacteria and Zymosan/Yeasts

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8
Q

What are the ligands and microorganisms recognized by TLR3?

A

Double-stranded viral RNA/Viruses e.g. West Nile virus

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9
Q

What are the ligands and microorganisms recognized by TLR4:TLR4 homodimer?

A

Lipopolysaccharide/Gram-negative bacteria

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10
Q

What are the ligands and microorganisms recognized by TLR5?

A

Flagellin/Motile bacteria having a flagellum

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11
Q

What are the ligands and microorganisms recognized by TLR7?

A

Single-stranded viral RNAs/Viruses e.g. HIV

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12
Q

What are the ligands and microorganisms recognized by TLR8?

A

Single-stranded viral RNAs/Viruses e.g. influenza

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13
Q

What are the ligands and microorganisms recognized by TLR9?

A

Unmethylated CpG-rich DNA/Bacteria and Viruses e.g. herpes viruses

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14
Q

What are the ligands and microorganisms recognized by TLR10?

A

Unknown

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15
Q

What is Nuclear Factor-kB (NF-kB)?

A

A transcription factor activated by TLR signals which promotes expression of various cytokines and endothelial adhesion molecules, important for inflammation.

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16
Q

What is Interferon Regulatory Factors (IFR)?

A

A transcription factor activated by TLR signals that stimulate the production of antiviral cytokines IRN-a/b called type I interferons.

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17
Q

Describe the TLR signaling cascade.

A

Ligand binds TLR. TLR —> Myd88 —> IRAK —> TRAF6 —> IKK —> NF-kB —> cytokines

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18
Q

What are NOD-Like Receptors (NLRs) and Inflammasomes?

A

NLRs are scaffolding proteins that make up the inflammasome after activated by pathogen. Inflammasomes activate protease capase-1 which process the inactive forms of IL-1B and IL-18 (cytokines) so they can be secreted.

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19
Q

Which NLR plays a key role in gout?

A

NLRP3

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20
Q

What are Damage-Associated Molecular Patters (DAMPs)?

A

Danger molecules released from damaged or dying cells. Triggers non-infectious inflammation.

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21
Q

How does necrosis and apoptosis differ in terms of DAMPs?

A

Apoptosis does not trigger the inflammation response as the apoptotic bodies containing DAMPS are removed by macrophages.

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22
Q

How does the DAMP, HMGB1, trigger inflamation?

A

Activates NF-kB via TLR2/TLR3 signaling.

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23
Q

How does the DAMP, uric acid, trigger inflammation?

A

Activates NF-kB via NLRP3.

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24
Q

How does the DAMP, heat shock protein, trigger inflammation?

A

Activates NF-kB via TLR2/TLR4.

25
Q

What do all DAMPs trigger the production of?

A

TNF-a and IL-1

26
Q

How can DAMP lead to an autoimmune disease?

A

Excessive triggering of DAMP inflammation promotes adaptive immunity, which can lead to responses against self-antigens.

27
Q

What is the significance of N-formyl methionyl peptide (fMet) in phagocytosis?

A

It is a typical PAMP that binds to the PRR formyl peptide receptor, activating chemotaxis. Phagocytes are localized to the area and initiate phagocytosis when encountering fMet.

28
Q

What antigen triggers the strongest immune response in macrophages?

A

Lipopolysaccharides (LPS)

29
Q

What is mast cells specialized in?

A

Amplification or suppression of innate or acquired immune responses. This can be done quickly because many of the secreted products are pre-formed.

30
Q

Where are mast cells commonly found and why?

A

They are common at sites exposed to the external environment, specifically in close proximity to blood vessels. This is so they can regulate vascular permeability and the recruitment of blood cells such as neutrophils and monocytes.

31
Q

What are the anti-inflammatory cytokines?

A

IL-10 and TGF-beta

32
Q

Which cytokine activates macrophages?

A

IFN-gama

33
Q

Which cytokines are involved in recruiting WBCs for the inflammatory response?

A

TNF-a, IL-1, IL-6, and IL-8

34
Q

What is the role of cytokine IL-12?

A

To activate NK cells and T helper cells, leading to macrophage activation.

35
Q

Which cytokines trigger sickness behavior syndrome?

A

TNF-aplha, IL-1, and IL-6

36
Q

Generally describe the complement system.

A

Initiated by 3 different pathways that all cause the same downstream effects. They all lead to the production of C3b, which activates C5. This creates a cascade that leads to the formation of the membrane attack complex (MAC) which lyses microbes.

37
Q

Describe how C3b is formed in the classical pathway.

A

C1 protein complex binds to antibodies on bacterial surface. C1 cleaves C2 and C4. C2a binds to surface-attached C4b, forming C3 convertase. C3 convertase cleaves C3a off of C3 and generates C3b.

38
Q

How is C5 convertase formed after the creation of C3b?

A

C3b forms a complex with C3 convertase to form C5 convertase.

39
Q

How is the membrane attack complex (MAC) formed from C5 convertase?

A

C5 convertase cleaves C5 into C5a and C5b. C5b initiates the self assembly of MAC (lytic pathway).

40
Q

What molecules make up the membrane attack complex (MAC)?

A

C5b, C6, C7, C8, and multiple molecules of C9.

41
Q

What is the clinical significance of C reactive protein (CRP) and SAA?

A

High concentrations detected means that there is inflammation.

42
Q

How are neutrophils tethered to endothelial cells?

A

TNF-alpha and IL-I activate endothelial cells to produce P-selectin (PS) and E-selectin (ES). PS and ES bind to PSGL-1 and ESL-1, respectively, which are both found on the surface of neutrophils.

43
Q

What are the 4 main steps for how neutrophils come into tissue?

A
  1. Tethering: PS and ES (selectins) binds ESL-1 and PSGL-1.
  2. Tight binding: interaction between integrins on neutrophils and integrin ligands on endothelial cells.
  3. Diapedesis: transmigration through endothelium.
  4. Chemotaxis: IL-8 controls migration of neutrophils in to inflammatory sites.
44
Q

Describe how the integrins on Neutrophils are activated.

A

LFA-1 and VLA-4 begin in low-affinity state. After the neutrophil binds to selectin, a chemokine (IL-8) also binds. The chemokine binds to its receptor and signals to activate LFA-1 and VLA-4, increasing their affinity for ICAM-1 and VCAM-1, respectively.

45
Q

What are the integrins fond on the surface of neutrophils and what do they bind to?

A

LFA-1 and VLA-4. They bind to ICAM-1 and VCAM-1 respectively.

46
Q

How is transmigration of monocytes different from neutrophils?

A

Monocytes use MCP-1 as their chemokine instead of IL-8.

47
Q

What is the difference between the classical and alternative pathways for macrophage activation?

A

Classical: M1 macrophages induced by TLRs and IFN-gamma. Used in microbicidal and proinflammatory response.
Alternative: M2 macrophages are induced by IL-4 and IL-13. Used in tissue repair and fibrosis.

48
Q

Describe the respiratory burst that accompanies phagocytosis.

A

Oxygen consumption is increased. Superoxide anion is produced, then converted to hydrogen peroxide (H2O2) by superoxide dismutase due to its instability. H2O2 broken down by myeloperoxidase into hydroxy radicals and hypochlorite.

49
Q

What are the 3 ways that Type 1 interferons (α/β IFNs) interfere with virus replication inside a host cell?

A
  1. Uses protein kinase RNA-activated (PKR) to prevent the recycling of guanidine diphosphate, blocking viral RNA translation.
  2. Activate Ribonuclease L which degrades viral RNA.
  3. Activate NK cells to eliminate infected cells.
50
Q

What interferon is produced by NK cells?

A

IFN-γ, the most powerful activator of macrophages to kill phagocytized microbes.

51
Q

Describe how NK cells are activated.

A

NK cells have activating receptors (KARs) and inhibitory receptors (KIRs). KARs bind to stress molecules MICA and MICB on the surface of abnormal host cells, triggering activation of protein tyrosine kinases (PTKs). KIRs bind to class I MHCs, activating protein tyrosine phosphatases (PTPs). If insufficient KIR binding occurs, NK cell will kill target host cell and vice versa.

52
Q

How do NK cells kill and infected cell?

A
  1. Release perforins to form hole in cell.
  2. Granzyme enter perforin hole and activates apoptosis.
  3. Macrophage engulfs dying cell.
53
Q

What are the 3 signals used for T cell activation?

A
  1. Recognition of antigen
  2. Costimulatory molecules expressed on APCs
  3. Cytokines produced by innate immune cells.
54
Q

Describe how PRRs activate T cells.

A

PRRs cause activation and maturation of APCs. APC processed antigen is presented to naive T cells. Secreted cytokines assist the development and maturation of T cells.

55
Q

What is the only TLR that is not involved in the cascade involving Myd88?

A

TLR3

56
Q

What is the role of C3a and C5a once they are broken off of their respective molecules?

A

Inflammation and chemotaxis

57
Q

How does the alternative complement pathway differ from the classical?

A

The alternative pathway involves the spontaneous activation of C3 (does not need IgM or IgG)

58
Q

What is protein kinase RNA-activated and how does it work?

A

Activated by Type 1 IFNs. Prevents the recycling of guanidine diphosphate which blocks viral RNA translation.

SFM Quiz 2 (15 decks)

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