IMMUN: Innate Immunity Flashcards
1
Q
characteristics of innate immunity
A
- same response and response lvl for all pathogens
- rapid response
- no immunological memory
- receptors are germline encoded (present on all cells)
2
Q
characteristics of adaptive immunity
A
- specific response
- diff response and response lvl for each pathogen
- immunological memory
- receptors on plasma membrane of lymphocytes (somatic encoded)
3
Q
anatomical barriers
A
- intact skin
- mucous membranes e.g. respiratory, GIT, genitourinary tract
4
Q
how does skin act as a barrier
A
- intactness + tight junctions: prevents entry
- normal flora
- fatty acids + lactic acid > hostile environment
5
Q
mechanical barriers
A
- mucociliary escalator
- coughing + sneezing
- vomiting + diarrhoea
- flushing e.g. sweat and tears
6
Q
chemical barriers
A
- acids: lactic acid (skin, vagina) and HCl/pepsin (stomach)
- antimicrobial substances e.g. lysozyme
- chemokines: attract phagocytes to infection site
- complement proteins
7
Q
antimicrobial substances produced by the body
A
- defensins: made by epithelial cells + leukocytes
- cathelicidins: made by macrophages, neutrophils and epithelial cells > specifically bind to microbial components e.g. LPS
- cytokines e.g. interleukins + interferons
- complement proteins
- lysozyme (destroys peptidoglycan cell walls) e.g. saliva, tears, sweat
8
Q
complement proteins: 3 pathways and function
A
- classical
- alternative (lipopolysaccharide trigger)
- lectin (starts w/ mannose binding lectin proteins)
- F = cell lysis through membrane attack complex (MAC) - causes water to come in and burst, opsonisation (flagging for phagocytosis) and recruiting phagocytes
- circulate blood in an inactive state
- can recognise pathogens
- pathways converge at C3
9
Q
WBCs involved in innate immunity
A
- phagocytes: neutrophils, monocytes, dendritic cells, macrophages
- granulocytes: basophils, mast cells, eosinophils
- NK cells
10
Q
what is the most abundant type of WBC?
A
- neutrophils
11
Q
what is pus made of?
A
- large numbers of neutrophils, tissue cells + dead pathogens
12
Q
NK cells: function, regulation
A
- recognise missing or non-self MHC I markers
- kill virally infected/cancer cells by secreting perforin to make holes in cell membrane > apoptosis
- activating receptors tell it to kill a cell, inhibitory receptors tell it to not kill it
- enhanced by macrophages and dendritic cells (+ve feedback)
13
Q
eosinophils and basophils
A
- release granules
- cytokines, histamines etc
14
Q
how is inflammation triggered?
A
- pro-inflammatory cytokines signal to endothelial cells to make them leaky to fluid and sticky for WBC so they can roll along and come out
- can also be triggered by complement activation or coagulation
15
Q
fever (pyrexia)
A
- body temp above 37˚C
- speeds up recovery b/c some immunological reactions are sped up by temperature
- can also provide hostile environment for some pathogens
16
Q
microbiota: what is it, what tissues should be sterile?
A
- outcompete pathogens or produce compounds that are toxic to pathogens
- internal tissues e.g. brain, blood, CSF, lower resp tract, upper urinary tract should be sterile
17
Q
mutualism
A
- both organisms benefit
- e.g. humans and microflora
18
Q
commensalism
A
- one benefits and one is unaffected
- some microflora
19
Q
parasitism
A
- one benefits and the other is harmed
- e.g. pathogens
20
Q
carrier vs chronic carrier of pathogen
A
- acute carrier: when pathogen is incubating, active or convalescent (post infection)
- chronic carrier: harbours pathogen for long periods, asymptomatic but can still transmit
21
Q
gut dysbiosis
A
- dis-regulation of microflora in gut due to less diversity or less number
- leaves host vulnerable to opportunistic infections
- increased inflammation
22
Q
opportunistic infection
A
- when normal flora become pathogenic if conditions or vulnerability changes
e.g. candida and S. aureus
23
Q
neutrophils
A
- multi-lobed nucleus
- granulocytes
- found in blood and migrate out during inflammation
- die after phagocytosis
- can undergo degranulation (release toxic granules), phagocytosis, neutrophil extracellular traps (webs of DNA coated w/ toxic granules)
24
Q
monocytes
A
- found in blood
- migrate into tissues and differentiate into macrophages
- can undergo phagocytosis, production of inflammatory mediators, antigen presentation
25
Q
what are macrophages and what are the 2 types
A
- found in tissues, made from monocytes (precursors)
- classically activated macrophage (M1): inflammatory
- alternatively activated macrophage (M2): anti-inflammatory (healing and repair): proline, polyamines, TGF-B
26
Q
how are NK cells activated
A
- usually, inhibitory receptor binds to MHC I on cells
- viruses turn off MHC I gene > NK inhibitory receptor can’t bind
- so then it kills cell
27
Q
how do innate immune cells recognise pathogens?
A
- detect PAMPs and DAMPs (damage-associated) using pattern recognition receptors (PRRs)
- e.g. lipopolysaccharides in gram-negative bacteria
28
Q
3 types of pattern recognition receptors (PRRs)
A
- toll-like receptors: on cell surface and in endosomes
- rig-like receptors: recognise viral RNA (cytosol)
- nod-like receptors: recognise PAMPs and DAMPs (cytosol)
29
Q
what do type I interferons do?
A
- inhibit viral replication
- enhance NK’s ability to kill virally infected cells
30
Q
chemokines
A
- cytokines that promote cellular movement
31
Q
3 ways that cytokines can act
A
- autocrine: on the releasing cell
- paracrine: on nearby cells (involves secretion of a ligand into ECF which binds to receptor on target cell)
- endocrine: travel thru bloodstream and act on cells that are further away
32
Q
local effects of cytokines
A
- endothelial: increase permeability, decrease flow rate, increased chemokine
33
Q
systemic effects of cytokines
A
- liver: increased acute phase proteins
- hypothalamus: increased body temp
- bone marrow: increased neutrophil production
34
Q
leukocyte migration process (diapedesis)
A
- macrophage (in tissues) recognises PAMPs via PRR > secretes cytokines and chemokines
- endothelial cells secrete selectin and integrin
- WBC slows down and rolls along endothelium (selectin mediated - ‘yellow light’)
- WBC binds tightly to endothelial cells (integrin mediated - ‘red light’), adheres to proteoglycans on endothelial cells
- leukocytes stop and squeezes thru vessel wall > move to infection site, following chemokine gradient
35
Q
3 types of TLRs
A
- type of PRR
- TLR 3 - found inside cell (recognise dsRNA in viruses)
- TLR 4 - found on cell membrane (recognise lipopolysaccharide in bacterial cell wall)
- TLR 5 - found on cell membrane (recognise flagellin protein in bacteria)
36
Q
phagocytosis process
A
- phagocyte PRR interacts with pathogen PAMP
- phagocyte engulfs pathogen by endocytosis > phagosome
- phagosome fuses with lysosome > phagolysosome
- reactive oxygen species, enzymes, other antimicrobial substances are released and digest the pathogen
37
Q
pro-inflammatory complement proteins and cytokines
A
- C3a and C5a
- IL-1, TNF-a
38
Q
what does C3b do?
A
- coat the pathogen, making it easier to phagocytose
- opsonisation
39
Q
what does C5b do?
A
- form the MAC with complements 6-9
40
Q
inflammasome
A
- found in myeloid cells
- triggered by damage, stress, or Fe fluctuations
- triggers inflammation through the promotion of IL-1
41
Q
what is a granuloma?
A
- connective tissue structure used to contain a pathogen
42
Q
after PRRs recognise PAMPs of a virus, which cytokines mediate an antiviral state?
A
IFN-a and IFN-B
