Innate Immunity Flashcards

(16 cards)

1
Q

Which type of immunity has Toll-like receptors, mannose receptors and NOD-like receptors? How do the cells get these receptors?

A

Innate, they are coded in germline of cell.

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2
Q

Which type of immunity has TCR receptors? How do they get them?

A

Adaptive. produced by somatic recombination of gene segments. More diversity than innate.

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3
Q

What are Defensins and cathelicidins and where does it fit into immunity?

what produces them?

A

antimicrobials. Part of the chemical barrier in innate immunity. Kills bacteria, virus, fungi with local abx

Neutrophils and Paneth cells

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4
Q

Where do you find Pattern Recognition Receptors (PRR)?

A

Innate immunity. Extracellular, Cytosolic and endosomal.

Born with these, recognized about 1,000 patterns
ex. Pilin, flagellin, LPS, ssRNA, CpG, Lipoteichoic acid, glucans, mannan

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5
Q

Which TLR are on extracellular of leukocytes? which are endosomal?

A

Extracell- TLR 1, 2, 4, 5, 6
Endosomal- TLR 3, 7, 8, 9

NOD like- similar but cytosolic.

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6
Q

What happens when a TLR finds a pathogen?

A

Increase microbicidal activity and apoptosis.

Produce defensins

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7
Q

What is the goal of the TLR signaling pathway?

What two transcription factors does it activate?

A

Promote inflammation and/or antiviral state.

  1. NF-kB > increase cytokines, adhesion molecules, costimulators > acute inflammation, stimulate adaptive immunity.
  2. IRFs (Interferon regulatory factors) > produce IFN a, B (Type I) > Antiviral state, send signal to other cells to creat barrier so not infected.
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8
Q

What is DAMP?

A

Damage-associated Molecular Patterns, (danger signal)

released by necrotic cells. Promote inflammatory response

Increase in serum levels of DAMPs associated with many inflammatory diseases: sepsis, arthritis, atherosclerosis, lupus, Chron’s, Cancer.

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9
Q

Macrophages release these, what do they do?

IL-1B and TNF-alpha
IL-6
CXCL8
IL12

A

IL-1B/TNFalpha: induce blood vessels to be more permeable, allowing effector cells to enter infected tissue.

IL-6 Induce fat/muscle cell to metabolize, make heat and raise the temp in the infected tissue

CXCL8: Recruit neutrophil from blood, guide to tissue

IL12: Recruits and activates NK cells which secrete cytokines to increase response of macrophage to infection

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10
Q

What is Chronic Granulomatous disease?

A

Usually Neutrophils kill microbes with pH, enzymes and ROS

In chronic granulomatous disease neutrophils can’t kill what they ate (genetic defect)

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11
Q

What do mast cells secrete? and what does it do?

A

Mast cells secrete histamine (vasodialator), amplifies inflammation

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12
Q

What do Natural Killer cells secrete? What does it do?

A

IFN-y: activates macrophages.

IL 12 is released from macrophages and recruites/activates NK cells

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13
Q

TNF-alpha, Normal and systemic

A

Usually cause inflammation (increase permeability.. )

Systemic infection (sepsis): macrophage release TNFalpha into blood stream > systemic edema > too much plasma out of blood > decrease blood volume, hypoproteinemia and neutropenia > collapse of vessels > Disseminated Intravascular coagulation leads to waisting and multiple organ failure: septic shock.

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14
Q

What do IFN-a and IFN-B (cytokines) do?

A

Triggered by virus infected cell.
Induce resistance to viral replication in all cells.
Increase expression for ligand for receptors on NK cells.
Activate NK cells to kill virus-infected cells.

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15
Q

Leukocyte Adhesion Deficiency I

What is going on and what are the symptoms?

A

IL-1 and TNF increase expression of P & E selections on endothelium, bind and slowing down (rolls) leukocytes so cytokines can hit it stimulate migration.

In LAD I integrin on leukocyte is deficient, can’t attach to endothelial receptors, no migration to infected site

Symptoms:
Delayed separation of umbilical cord. 
recurrent bacterial infections, in skin and mucosa 
Leukocytosis
Periodontitis (later)
Impaired wound healing
Absent pus formation.
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16
Q

What is contraction? What players are involved (4)?

A

When pathogen is cleared, need to heal and decrease inflammation

IL-10
IL-1 receptor antagonist
Suppressor of cytokine signaling (SOCS) proteins
Alternative C’ pathway inhibitors