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HDM Midterm - Brett > Activation of Innate Immunity > Flashcards

Activation of Innate Immunity Flashcards

1
Q

What are the regulatory cytokines and what are they responsible for?

A

TGF-beta allows repair without regulatory immune cells

IL-10 secreted by macrophages, dendritic cells, and Tregs

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2
Q

What are the endogenous pyrogens?

A

IL1, IL6, TNF-alpha

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3
Q

What causes SIRS?

A

Systemic inflammatory response syndrome ==> too many IL1, IL6, TNF-alpha

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4
Q

What causes fever?

A

Hypothalamic response to IL1, IL6, TNF-alpha

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5
Q

What does fever cause?

A
  1. Bacterial and viral replication decreased at higher temperature
  2. Antigen processing is enhanced
  3. Adaptive immunity becomes more potent
  4. Cells become more resistant to TNF-alpha activity by down-regulating receptor
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6
Q

What activates acute-phase proteins?

A

IL6

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7
Q

What acute-phase proteins are activated in response to infection?

A

C-reactive protein — binds to phosphorylcholine on bacteria and acts to activate complement and functions as opsonin

Mannose-binding lectin — binds to residues on bacteria; activates complement and acts as opsin

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8
Q

What acts as a non-specific cue for acute inflammation?

A

C-reactive proteins

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9
Q

What are the the systemic pathologic effects of pyrogens?

A

Low cardiac output, increased permeability, insulin resistance in multiple tissues

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10
Q

Where is complement produced?

A

Hepatocytes

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11
Q

Is complement part of innate or adaptive immunity?

A

Innate

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12
Q

Classical pathway of complement causes what 3 actions?

A
  1. Simulates inflammation
  2. Facilitates antigen phagocytosis
  3. Can lyse some cells directly
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13
Q

What is the aternative complement pathway called?

A

Lectin complement

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14
Q

The alternative or lectin C’ pathway begins with…

A

C3 spontaneous cleavage to C3b and C3a, C3b binds to microbe and acts as an opsin, C3b causes C5 to cleave into C5b and C5a which can lead to MAC

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15
Q

What does MAC stand for?

A

Membrane attack complex — it creates a pore to cause cell contents to leak

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16
Q

What are the anaphylatoxins and what do they do?

A

C3a, C4a, C5a and they have inflammatory activity, they are also by-products of complement activation

Induce SM contraction
Induce mast cells/basophils to release inflammatory mediators of histamine and vasodilators which increase capillary permeability

17
Q

What is the most potent anaphylatoxin?

A

C5a

18
Q

What increases the expression of selectins and what do selectins do?

A

IL1 and TNF, selectins allow luekocyte to roll and eventually stop

19
Q

What causes integrin to transition to high affinity state?

A

IL-8

20
Q

What causes cytoskeletal changes in leukocytes so they can complete extravasation

A

LFA 1 on neutrophil binding to endothelial ICAM1

21
Q

How do neutrophils and macrophages eventually find their target?

A

Chemokine gradient

22
Q

The acute inflammatory response has 3 steps, what are they?

A
  1. Vasodilation (degranulate mast cells, dendritic cells, and macrophages)
  2. Increased vascular permeability (TNF/IL1/IL6)
  3. Emigration of leukocytes to site of damage (follow chemokines)
23
Q

What is the kinin cascade? What does it do?

A

It is part of the inflammatory response and causes vasodilation, increase permeability of blood vessels, and stimulate pain receptors

24
Q

What is the fibrinolytic protein?

A

This degrades the clot when the wound has healed

25
Q

What is a rebuck skin window?

A

The skin tissue is lightly damaged until there is some oozing —> every 2 hours the slide cover over this damage is removed and viewed under the scope

26
Q

What are the two types of LAD? What are they? What does LAD stand for?

A

Adhesion defect (1 and 30 and rolling defect (2)

Leukocyte adhesion deficiency

27
Q

Low levels in ________ cause low or no CD11a, 11b, 11c in the cell membrane

A

CD18

28
Q

LFA has to do with the migration of what?

A

Neutrophils

29
Q

Mac-1 has to do with the migration of what?

A

T cell migration

30
Q

What are some clinical signs of LAD?

A

Omphalitis, recurrent infections in skin and mucosal tissues (neutrophils can’t migrate), elevated white count (more cells are made but they can’t properly arrive), no pus formation, impaired wound healing, periodontitis later in life

31
Q

What organism shows resistance to phagocytosis

A

Pneumococci

32
Q

What shows resistance to ROS

A

Staphylococci

33
Q

Resistance to complement activation

A

Neisseria meningitidis and streptococci

34
Q

What has resistance to antimicrobial peptide antibiotics?

A

Pseudomonas

35
Q

What is the timeline which we switch from innate to adaptive

A

5 days

HDM Midterm - Brett (10 decks)

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