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IMMUNOLOGY VDMP817 > lecture 2 > Flashcards

lecture 2 Flashcards

1
Q

key functions of innate immunity

A
  1. prevent, control and eliminate infectious agents
  2. recognize and eliminate products of damaged/dead host cells -> initiate tissue repair
  3. stimulate and influence adaptive (special) immune repsonse
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2
Q

components of innate immunity

A 
mechanical barriers
chemical barriers
physiological factors
proteins
cells
initiates adaptive immune response
disruption of innate immunity by microbes :(
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3
Q

mechanical barriers

A

intact skin
mucosal epithelia & mucus (sneezing, coughing, vomiting, diarrhea)
shedding of infected skins
flushing of bodily fluids (tears, saliva, sweat, pee)

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4
Q

chemical barriers

A

skin (sebum - sweat)
saliva (lysozyme and antibiotics
mucus (lysozyme and antibiotics)
tears (lysozyme)
DEFENSINS (alpha, beta and gamma - within skin, mucosal epithelial cells, neutrophils and NK cells)
CATHELICIDINS (neutrophils, skin epithelia, GI/respiratory mucosa - will poke hole in pathogen mwhaha)
LACTOFERRIN (bind to iron to create stabber for microbe… decreases RBC production, acute phase protein)
HCl (in stomach)
bile salts and acids

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5
Q

physiological factors

A

temperature (high fever reduces growth for microbes)
oxygen tension (high O2 makes anaerobic microbes die)
hormonal balance (corticosteroids lead to decreased inflammatory response which could lead to infection)
age (kids and gpas at higher risk to disease bc suboptimal immune systems)

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6
Q

effector proteins

A 
complement
mannose binding lectin
c reactive protein
cytokines (TNF, IL-1, chemokines, IFNalpha, IFNbeta, IFNg, IL12, IL15, IL10, TGFb, IL8)
natural antibodies
acute phase proteins (lactoferrins)
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7
Q

complement effector protein

A

kills microbes
opsonization of microbes (through initiating phagocytosis)
activation of leukocytes (WBC)

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8
Q

opsonization

A

extracellular protein that signals to phagocytizing cell to eat it and KILL, tag cells for phagocytosis

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9
Q

mannose binding lectin

A

collectin
binds carbohydrates
opsonization of microbes
activation of complement -> lectin pathway

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10
Q

C reactive protein

A

pentraxin
osponization of microbe
activation of complement

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11
Q

TNF, INL1, chemokines

A

inflammation

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12
Q

IFNa & b

A

resistance to viral infection

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13
Q

IFNg

A

macrophage activation (macrophage cant kill microbe unless activated!)

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14
Q

IL12

A

NK and Tcells make IFNg (macrophage activation!)

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15
Q

IL15

A

proliferation of NK cells

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16
Q

IL10, TGFb

A

control inflammation

17
Q

IL8

A

CXCL8 - chemokine

chemoattractant of neutrophils

18
Q

natural antibodies

A

made by B cell from fetal liver stem cells (hemopoetic)

19
Q

acute phase proteins

A

lactoferrin

inflammation

20
Q

alarmins

A

inflammatory molecule as result of damaged cell/tissue
heparan sulfate (repair ECM)
heat shock proteins (repair cytoplasm?)

21
Q

vasoactive lipids

A

inflammatory molecule as result of damaged cell/tissue
prostaglandins
leukotrienes

22
Q

generation of vasoactive lipids from cell membrane

A

damage to cell/tissue -> phospholipases activated -> cell membrane phospholipids broken -> arachidonic acid -> a. leukotriene -> b. prostaglandin
results in increased vascular permeability and smooth muscle contraction (swelling) or pain and vasodilation
5-lipoxygenase (enzyme for leukotriene)
cycloozygenase (enzyme for prostaglandin)

23
Q

aspirin inhibits

A

cyclooxygenase -> so the pain and vasodilation response of prostaglandins is inhibited

24
Q

steroids inhibit

A

phospholipase -> so the entire vasoactive lipid pathway is disrupted, no swelling or pain response

25
Q

LTB4

A

leukotriene that is involved in chemotaxis for blood leukocytes (neutrophils and eosinophils)
aka triggers cell responders to come kill

26
Q

LTC, LTD, LTE

A

leukotriene that increases vascular permeability and smooth muscle contraction aka swelling

27
Q

neutrophil

A

effector cell (innate inflammatory response)
early phagocytosis
kills microbes
10^11 produced daily, in instance of infection there are lots of neutrophils produced

28
Q

macrophage

A

effector cell - sentinel
secondary phagocytosis to finish the job of neutrophil
kills microbes
secretes cytokines that stimulate inflammation
antigen presenting to T cell!! shows antigen after killing the pathogen which is helpful for future response)

29
Q

NK cell

A

lysis of infected cell

activates macrophage through secretion of INFg

30
Q

sentinel cell

A

sense tissue damage and recognize microbes
induce inflammation (to localize the infection!)
recruit blood leukocytes via cytokines and chemokines
kill pathogens

31
Q

dendritic cell

A

sentinel cell
most important in antigen presenting
<1% of cell type in body
1. capture, process and present antigens to lymphocytes - PROFESSIONALLY - this is how primary immune response initiated
2. provide signals to stimulate T cell proliferation and differentiation
3. secrete cytokines and chemokines (attract leukocytes)
langerhans
interstitial DC
interdigitating DC
circulating DC

32
Q

mast cell

A

sentinel cell
secrete: vasoactive amine (histamine & serotonin -> increase vascular permeability & pain) & inflammatory proteins (like cytokines which attract blood leukocytes)

33
Q

PAMPS

A

pathogen associated molecular patterns (for recognition done by sentinel cells)
- conserved molecular motifs found ON THE microbes (their signatures) -> stimulate a specific innate immune response once bind to recognition receptor
- detected by pattern recognition receptors (same receptor can bind different microbes
nucleic acids: virus’ and bacteria detecting
proteins: bacteria
cell wall lipids: gram - bacteria
carbohydrates: fungi, bacteria

34
Q

pattern recognition receptor

A

can be found in:
soluble (collectins, ficolins, complement, pentraxins)
w/in vesicles (TLR3, 7, 8, 9) - can sense the presence of pathogen from endosome
cytoplasmic (Rig1, NOD like, peptidoglycan receptors, DNA receptors - detect the pathogens PAMPS that hide in cytoplasm)
membrane bound (TLR, lectin, mannose receptor, langerin, dectin, scavenger receptors, integrins - allow cell to recognize an extracellular pathogen)

35
Q

DAMPS

A

damage associated molecular patterns produced from stressed of injured host cells
stress induced (heat shock protein)
crystals (monosodium urate)
nuclear proteins (HMGB1 - high mobility group box 1 protein - nuclear proteins that are present around the chromosome)

36
Q

PAMP-PRR binding

A

example: LPS (gram - molecular pattern) binds to TLR4 cell membrane protein to signal cytokine release

DAMP disruption activates HMGB1 to trigger endothelium, neutrophil (inflammation -> tissue damage -> shock), macrophages, dendritic cells and epithelium

37
Q

EqStim

A

medication that can be used to activate sentinel cell killing mechanisms
prime horses with injection prior to shipping and reduces respiratory infection

same with zelnate

38
Q

innate vs adaptive

A

innate: specific for structures shared by groups of related microbes, limited diversity - sticks to germline, no memory, and in not reactive to self
adaptive: specific for antigens of microbes and nonmicrobial antigens, very diverse - receptors are produced by somatic recombination of gene segments, does have memory!, not reactive to self

IMMUNOLOGY VDMP817 (22 decks)

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