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SFM (Scientific Foundations of Medicine) > Lecture 19: Innate Immunity > Flashcards

Lecture 19: Innate Immunity Flashcards

1
Q

5 cardinal signs of Inflammation

A
  1. Heat
  2. Redness
  3. Swelling
  4. Pain
  5. Loss of Function
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2
Q

Fever

A
  • from strong proinflammatory response
  • not DIRECTLY caused by pathogenic factors
  • cytokines TNF, IL-1, IL-6 are potent inducers
  • most pathogens replicate poorly in elevated temps
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3
Q

What are PAMPs?

A
  • Pathogen-associated Molecular Patterns
  • unique to particular classes of pathogens
  • usually required for survival, cannot be hidden from surface
  • not similar to self-Ags
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4
Q

Gram- PAMPs

A

Porin, Lipopolysaccharide, Lipoprotein

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5
Q

Gram+ PAMPs

A

Teichoic acid, lipoteichoic acid, peptidoglycan, lipoprotein

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6
Q

Mycobacteria PAMPs

A

lipoarabinomannan, porin, lipoprotein

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7
Q

Fungi PAMPs

A

manno-proteins, B-glucan, lipoprotein

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8
Q

Extracellular TLRs and what they recognize

A

TLR 1/2 - bacterial lipopeptides

TLR 2 - bacterial peptidoglycans

TLR 4 - LPS

TLR 5 - bacterial flagellin

TLR 2/6 - bacterial lipopeptides

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9
Q

Intracellular (endosome) TLRs and what they recognize

A

TLR 3 - dsRNA

TLR 7 - ssRNA

TLR 8 - ssRNA

TLR 9 - CpG DNA

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10
Q

MyD88, TRIF, IRF, NK-kB

A

MyD88 - activated by all TLRs, cause NK-kB/IRF act.

TRIF - activated by TLR3/4, cause NK-kB/IRF act.

IRF/NK-kB - transcriptional factors

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11
Q

TLR Deficiencies (MyD88 and IRAK-4 deficiency)

A
  • defective TLRs = innate immune cell cannot kill microbe
  • signaling defects = failure to produce cytokines

MyD88/IRAK-4 def: susceptibility to infection either by bacteria or viruses

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12
Q

Inflammasomes and NOD-like Receptors

A

NLR - scaffolding for signaling platform that activates NF-kB and MAPK pathway

Inflammasome - activates protease caspase 1
- process inactive cytokine precursors into active form (IL-1B and IL-18)

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13
Q

What two cytokines drive inflammation?

A

IL-1B and IL-18

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14
Q

NLRP3 Inflammasome and Gout

A
  • IL-1B is key cytokine in gout; promotes neutrophil influx into synovium and joint fluid
  • pathological hallmark of acute inflammatory attack
  • Anti-IL-1 therapy used to treat gout patients
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15
Q

Necrosis and DAMPs

A

Necrosis: dirty cell death; swelling and rupture of cell membrane, causing inflammation

  • strong DAMP release (endogenous danger molecules released from damaged/dying cells during NON-INFECTIOUS INFLAMMATION
  • DAMPs recognized by PPRs (pattern recognition receptors)
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16
Q

Major DAMPs that activate NF-kB (3)

A
  1. HMGB1 (high mobility group box 1)
    • receptor: TLR2/3
  2. Uric Acid
    • receptor: NLRP3
  3. Heat Shock Proteins
    • receptor: TLR2/4

ALL DAMPs stimulate TNF-alpha and IL-1 release

17
Q

What signals allow do phagocytes recognize that allow them to begin phagocytosis?

A
  • fMet via Formyl Peptide Receptor (PPR)
  • receptor involved in chemotaxis
  • phagocytes bind fMet bacterial proteins and use them to initiate phagocytosis
18
Q

IL-10 and TGF-beta

A

Anti-Inflammatory cytokines

19
Q

Sickness Behavior Syndrome

A
  • systemic release of TNF-alpha, IL-1. IL-6

- lethargy, depression, fever, cognitive impairment, decreased social interaction

20
Q

C3 convertase and roles of C3a/C3b

A
  • convertase: C4bC2a; cleaves C3 into C3a and C3b
  • C3a: inflammation, chemotaxis
  • C3b: phagocytosis, C5 convertase formation

CLASSICAL PATHWAY

21
Q

C5 convertase roles of C5a/C5b

A
  • convertase: C4bC2aC3b
  • C5a: inflammation
  • C5b: MAC formation
22
Q

What are CRP and SAA, and what do they help do?

A
  • both are acute phase proteins
  • C-reactive Protein and Serum Amyloid A show up in 100x increase during inflammation
  • measurement of their levels helps diagnosis inflammation
23
Q

Steps for Neutrophil into tissues

A
  • TNF-alpha, IL-1 activate endothelial cells, which increase P and E selectin adhesion molecules
  1. Tethering - slow down/roll on epithelium
    • P/E selectin and PSGL-1/ESL-1 mediated
  2. Tight Binding - integrin interactions (LFA-1/VLA-4 on neutrophil, ICAM-1/VCAM-1 on endothelial cells)
  3. Diapedesis - endothelium transmigration
  4. Chemotaxis - IL-8 controls migration to inflammatory sites
24
Q

What is the most important chemokine for monocyte migration/infiltration into tissues? What happens to monocytes once they get into tissue?

A

MCP-1 (monocyte chemoattractant protein-1)

  • become tissue macrophages; maturation controlled by cytokine microenvironment in tissue
25
Q

Classical vs Alternative Tissue Macrophage activation

A

Classical (M1): microbial TLR-ligands, IFN-y
- microbicidal and proinflammatory

Alternative (M2): IL-4 and IL-13
- tissue repair and fibrosis

  • play critical role in IMMUNOMODULATION
26
Q

Type I Interferons (a/B IFNs) (Anti-viral Innate Immune Response)

A
  • express proteins that interfere w/viral replication
  • PKR –> no GDP recycling; blocks viral RNA translation
  • Ribonuclase L –> viral RNA degradation
  • activate NK cells
27
Q

Natural Killer Cells (Anti-viral Innate Immune Response)

A
  • recognize ligands on infected/stressed cells and kills them (eliminates reservoir of infection)
  • killing ability inversely related to expression of MHC 1 on target cells (MHC present = PTK dephosphorylation = inactivation)
  • produce IFN-y, activate macrophages
  • use perforins and granzymes
28
Q

What stress-associated molecules do NK Cells recognize on the surface of abnormal host cells?

A

MICA and MICB

SFM (Scientific Foundations of Medicine) (20 decks)

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