Activation of Innate Immunity Flashcards Preview

HDM Midterm - Brett > Activation of Innate Immunity > Flashcards

Flashcards in Activation of Innate Immunity Deck (35):
1

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

TGF-beta allows repair without regulatory immune cells

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

2

What are the endogenous pyrogens?

IL1, IL6, TNF-alpha

3

What causes SIRS?

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

4

What causes fever?

Hypothalamic response to IL1, IL6, TNF-alpha

5

What does fever cause?

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

6

What activates acute-phase proteins?

IL6

7

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

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

8

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

C-reactive proteins

9

What are the the systemic pathologic effects of pyrogens?

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

10

Where is complement produced?

Hepatocytes

11

Is complement part of innate or adaptive immunity?

Innate

12

Classical pathway of complement causes what 3 actions?

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

13

What is the aternative complement pathway called?

Lectin complement

14

The alternative or lectin C’ pathway begins with...

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

15

What does MAC stand for?

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

16

What are the anaphylatoxins and what do they do?

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

What is the most potent anaphylatoxin?

C5a

18

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

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

19

What causes integrin to transition to high affinity state?

IL-8

20

What causes cytoskeletal changes in leukocytes so they can complete extravasation

LFA 1 on neutrophil binding to endothelial ICAM1

21

How do neutrophils and macrophages eventually find their target?

Chemokine gradient

22

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

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

What is the kinin cascade? What does it do?

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

24

What is the fibrinolytic protein?

This degrades the clot when the wound has healed

25

What is a rebuck skin window?

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

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

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

Leukocyte adhesion deficiency

27

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

CD18

28

LFA has to do with the migration of what?

Neutrophils

29

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

T cell migration

30

What are some clinical signs of LAD?

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

What organism shows resistance to phagocytosis

Pneumococci

32

What shows resistance to ROS

Staphylococci

33

Resistance to complement activation

Neisseria meningitidis and streptococci

34

What has resistance to antimicrobial peptide antibiotics?

Pseudomonas

35

What is the timeline which we switch from innate to adaptive

5 days