Inflammation: Soluble and Cellular Effector Mechanisms in Innate Immunity Flashcards

1
Q

Inflammation:

A

A physiologic process by which vascularized tissues respond to injury.

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2
Q

Chronic inflammation:

A

Longer duration than acute.
Accumulation of fluid, plasma proteins and neutrophils –> influx of lymphocytes, macrophages and possibly ending in fibroblast growth. May result in granuloma.

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3
Q

Prostaglandins:

A

Oxidative derivative of fatty acid that mediates signs of inflammation (fever, pain, vascular permeability)

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4
Q

Leukotrienes:

A

Inflammatory mediators derived from oxidation of arachidonic acid. Mediate vasoconstriction, increased vascular permeability, endothelial adhesiveness and neutrophil chemotaxis.

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5
Q

IL-1/IL-6/TNF-alpha have effects on (4):

A
  1. Liver.
    - Acute-phase proteins.
  2. Bone marrow endothelium.
    - Neutrophil mobilization.
  3. Hypothalamus.
    - Increased body temperature.
  4. Fat, muscle.
    - Protein and energy mobilization.
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6
Q

Initiates the alternative pathway:

A

Pathogen surface + C3b

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7
Q

Initiates the lectin pathway:

A

Mannose-binding lectin

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8
Q

Initiates the classical pathway:

A

Antibodies IgG, IgM, IgA

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9
Q

Different compliment pathways converge at:

A

Cleavage of C3 —> C3a and C3b

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10
Q

C1-INH:

A

Soluble regulatory protein that acts on C1 in the classical pathway.

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11
Q

Factor I/Factor H:

A

Soluble regulatory protein that acts on C3-convertase.

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12
Q

CD55:

A

Membrane bound regulatory protein that acts on C3- and C5-convertase.
- Decay Accelerating Factor (DAF)

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13
Q

CD59:

A

Membrane bound regulatory protein that acts on the MAC.

- MAC-inhibitory protein.

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14
Q

PAMPS:

A
  • Pathogen Associated Molecular Patterns
  • Found on pathogens
  • Link to PRRs
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15
Q

TLRs:

A
  • Toll Like Receptors
  • Type of PRR
  • Can be on membrane or in endosome.
  • Turn on cytokines or interferon pathway.
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16
Q

Consequences of TLR to innate immunity (3):

A
  1. Secretion by macrophages and dendritic cells of cytokines.
  2. Improve phagocytosis by macrophages.
  3. Enhanced ability of dendritic cells to induce adaptive immunity.
17
Q

DAMPS:

A
  • Damage Associated Molecular Patterns
  • Not associated with pathogens.
  • From necrosis (not apoptosis).
  • Bind to PRRs
  • Promote and exacerbate acute inflammatory response.
18
Q

Three sources of neutrophils:

A
  1. Circulating in the blood.
  2. Neutrophils stimulated to differentiate and mobilize from precursors in the bone marrow.
  3. Stores in venules (margination).
19
Q

Neutrophil response to chemokines:

A
  1. Margination, or rolling slowly along the blood vessel wall.
  2. Definitive sticking/adherence mediated by selectins and intergrins.
  3. Pass through gaps in endothelial cells (diapedisis).
  4. Migrate to inflammatory site.
20
Q

Extravasation:

A

Passage of cells from interior of blood vessels to the extravascular space.

21
Q

Actions of interferon alpha and beta (3):

A
  1. Inhibiting viral replication.
  2. Inhibit viral binding to neighboring cells.
  3. Eliciting and activating NK cells to deliver a “lethal hit”.
22
Q

To induce eosinophil degranulation helper T cells release (3):

A
  1. IL-5
  2. IL-3
  3. GMCSF
23
Q

Growth factors for mast cells (3):

A
  1. IL-3
  2. IL-5
  3. GMCSF
24
Q

Mast cells have high affinity Fc receptor for:

A

IgE

25
Q

Glucocorticoids:

A
  • Produced by adrenal cortex.
  • Immunosuppression.
  • Down-regulate inflammation.