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MBB311 - Molecular Immunology > Innate Immunity > Flashcards

Innate Immunity Flashcards

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1
Q

name 3 forms of physical barrier and state where they are found

A

1) epithelial cells joined by tight junctions (skin, GI, UG, resp)
2) flow of air/fluid (skin, UG, GI, resp)
3) cilia (resp)

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2
Q

name 4 chemical barriers and state where they are found

A

1) fatty acids (skin)
2) low pH enzymes eg pepsin (GI and UG)
3) lysozyme - breaks down peptidoglycan (resp)
4) antibacterial peptides - create pores in pathogen walls (defensins) (everywhere)

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3
Q

name 3 types of antimicrobial peptide and state what they do

A

defensin - disrupts plasma membrane
cathelicidin - disrupts PM (released by neutrophils and macrophages in response to keratinocyte infection)
histatins - active against fungi in oral cavity

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4
Q

name the central event in the complement system. what enzyme catalyses this?

A

C3 –> C3a + C3b

C3 convertase

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5
Q

name 3 complement pathways

A

classical
mannose-binding lectin
alternative

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6
Q

name the 3 c3 convertases in each complement pathway

A

classical: C4bC2a
MBL: C4bC2a
alternative: C3bBb

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7
Q

how is the MBL pathway stimulated?

A

MBL binding to pathogen surface (trimerises –> oligomerizes = avidity)
or ficolin binding to pathogen
overall: a PRR (ficolin/MBL) recog a PAMP on pathogen

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8
Q

briefly describe the MBL pathway

A 
MBL/ficolin + MASP complex + pathogen 
activated MASP1
cleaved and activated MASP2
cleaved and activated C4 and C2
formation C4bC2a C3 convertase
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9
Q

what property of C3b and C4b allows them to bind pathogen? why is this useful in regulation?

A

cleavage of C3 exposes a thioester on C3b (same for C4 and C4b) which can covalently bond OH/NH2 on pathogen. if no pathogen around, thioester rapidly hydrolyzed = inactivation C3b/C4b

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10
Q

how is the classical pathway stimulated?

A

C1q direct binding to pathogen
OR
C1q binding Ab-pathogen (more efficient)

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11
Q

briefly describe the classical pathway

A 
C1q (+Ab) + pathogen
conformational change in c1r/c1s
activated c1r
cleaved and activated c1s 
cleaved and activated c4 and c2
formation c4bc2a c3 convertase
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12
Q

how is the alternative pathway stimulated?

A

C3b generated by classical/MBL pathway
C3b can bind factor B
C3 undergoes spontaneous hydrolysis (tickover) which binds factor B

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13
Q

briefly describe both versions of the alternative pathway

A

C3b binds factor B
C3bB binds factor D
factor D cleaves factor B to form C3bBb + Ba
formation of C3bBb C3 convertase OR
C3 spontaneous hydrolysis: C3(H2O) binds factor B
C3(H2O)B cleaved and activated by factor D which produces C3(H2O)bBb+Ba
formation of C3 convertase: C3(H2O)bBb

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14
Q

describe the opsonin action created by the complement system

A

C3b cov bonds to pathogen (via thioester)

phagocytes with C3b receptor ingest complement covered pathogen more efficiently

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15
Q

describe the chemoattractant action created by the complement system

A

C3b binds C5 convertase

C3a+C5a = chemoattractant which recruits phagocytes (inflammation)

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16
Q

describe how the complement system can activate the MAC

A

C5b generated by C3b triggers late events of complement system
C5bC6C7 binds pathogen membrane
C8 binds and inserts into membrane
C9 binds complex and polymerizes –> formation of MAC pore

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17
Q

how is the complement system regulated

A

thioester bond hydrolysis
components rapidly hydrolysed in fluid phase
regulatory proteins:
C1 inhibitor
carboxypeptidase N inactivates C3a and C5a
CD59 on host cells bind C9 - prevents MAC formation
factor H competes with C3b for factor B binding

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18
Q

why is complement important? which pathogens is it activate against?

A

important bc: interacts with adaptive immune system (classical), aids in clearing immune complexes, activates T&B cells
active against: extracellular bacterial and fungal infections and possibly against some viruses

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19
Q

name 3 types of sentinel cell

A

1) macrophages (therefore kupffer cells/langerhans cells/alveolar macrophages/microglia)
2) dendritic cells
3) mast cells

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20
Q

how do innate immune cells recog pathogens/pathogenicity

A

use PRRs to recog:
PAMPs (non-self)
DAMPs (damage to self cells)

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21
Q

name bacterial, fungal, viral and protozoan PAMPs

A 
bac: 
gram -ve: LPS
gram +ve: LTA
all: flagellins, un-meth CpG, N-formylated proteins
fungi: 
chitin
beta-glucans
viruses:
dsRNA
protozoa:
GPI-linked proteins
mannose-rich proteins
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22
Q

name some DAMPs

A

fragments of extracellular proteins
phosphatidylserine (inner leaflet of PM therefore apoptosis must have occured)
Heat shock proteins (abnormally associated with PM)
Mitochondrial components in cyt
uric acid (kidney damage/ oxphos stress)
DNA
HMGB1 (histone-like should be in nuc)

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23
Q

name the 3 classes of PRRs and give examples

A

1) soluble receptors (MBL/complement/ficolins/pentraxins)
2) membrane-bound receptors (complement receptors/scavenger receptors/lectin receptors/toll-like receptors/chemotactic receptors)
3) cytoplasmic receptors (NOD-like receptors)

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24
Q

name some effector functions of soluble receptor PRRs

A

identify non-self/altered-self
opsonins that facilitate engulfing and clearing of apoptotic cells
Neutrophil extracellular traps (NETs) contain g/mDNA which are targets for ficolins and pentraxins
SP-A and SP-D enhance clearance of pathogens by recruitment lung alveolar macs and antibodies respectively

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25
name some effector functions of membrane receptors
phagocytosis: c-type lectins recog beta-glucans in fungi mannose receptors recog mannose in bac/fungi/virus scavenger receptors recog anionic polymers (CD14 for LPS CD36 for LDL) chemotaxis: chemotactic receptors recog chemoattractants (eg f-MLP receptor for N-formylated proteins) signalling: Toll-like receptors (TLR-4 recog LPS when associated with MD-2 and CD14: LPS-CD14-TLR4 --> signalling) TLRs dimerise and recruit kinases and ubiquitin ligases to activate transcription of inflammatory genes
26
name some effector functions of cytoplasmic receptors
NOD-like receptors (NLRs) recog bac components eg flagellin/peptidoglycan, induction signalling and assembly inflammasomes RIG-1-like receptors (RLRs) recog viral RNA produced within a cell, signalling induces expression interferons
27
name 7 inflammatory mediators, give egs of them and explain how they work
1) lipid mediators: prostaglandins (breakdown phospholipids to allow fluid entry into tissue) 2) cytokines: TNF-alpha (activates endothelial cells --> increased vascular dilation and permeability) 3) chemoattractants: fMLP (stimulates macrophage presence) 4) complement proteins: C5a (activates local mast cells and causes release of granules) 5) Vasoactive amines: histamine/bradykinin (bradykinin increases vascular permeability, plasma proteins enter tissue) 6) clotting factors 7) small molecules: ROI, RNI (destroy pathogens)
28
describe the process of extravasation
1) cytokine signalling results in P-selectin production on endothelium. E-selectin is induced by TF-alpha/LPS presence on endothelium. Sialyl-Lewis X on macrophages interacts with selectins --> rolling of WBCs 2) cytokines induce endothelium to express adhesion molecules 3) integrins activated on WBCs and bind adhesion molecules (ICAM1/VCAM1) on endothelium 4) EXTRAVASATION - WBC crosses endothelium
29
what are cytokines? are they long or short range acting?
small glycoproteins 'hormones of IS' | paracrine (locally acting)
30
name the five groups of cytokines
1) interleukins (IL family) - req activation from inflammasome 2) hematopoietin superfamily - v large and varied 3) interferons 4) TNF family: mainly TM proteins that can be removed from PM 5) chemokines - 2 groups CC/CXC
31
what does IL1 do? which cells produce it?
activates macrophage and T cells and induces fever | made my macs, endothelial and epithelial cell
32
what does IL2 do? which cells produce it?
stimulates T cell growth and differentiation | T cells
33
what does IL4 do? which cells produce it?
``` induces class switching in IgE, promotes TH2 differentiation TH2 cells, mast cells ```
34
what does IL8 (CXCL8) do? which cells produce it?
induces neutrophil, basophil and T-cell chemotaxis to site of infection macrophages, endothelium, fibroblasts, keratinocytes
35
what does IFNgamma do? which cells produce it?
activates macrophages and NK cells, increases MHCII expression T cells, NK cells
36
what does TNFalpha do? which cells produce it?
promotes inflammation, endothelial activation (increased vascular permeability leads to increased entry of IgG, leukocytes and complement into tissue and well as increased drainage to lymph nodes), cachexia (wasting), fever (by acting on hypothalamus), microthrombus, influx platelets (clotting) T cells, macrophages, NK cells
37
what does GM-CSF do? which cells produce it?
production of granulocytes, macrophages, DCs | produced by T-helpers
38
what does TGFbeta do? which cells produce it?
anti-inflammatory | produces by monocytes and T cells
39
which cytokine receptors signal through enzyme-coupled receptor dimers?
homodimeric heterodimeric with a common chain heterodimeric with no common chain TNF
40
which cytokine receptors signal through G-proteins?
chemokine receptor family
41
what does IL1beta do? what are its systemic effects?
activates vascular endothelium, activated lymphocytes, local tissue destruction, increases access of effector cells systemic: fever, production of IL6
42
what does IL6 do? what are its systemic effects?
lymphocyte activation, increased antibody production | systemic: fever, induction acute phase protein production (proteins produced in response to inflammation)
43
what does IL12 do?
activated NK cells, induces differentiation of CD4 T cells into TH1 cells
44
what happens when [TNFalpha] > 1ug/ml?
SEPSIS widespread increase in vascular permeability disseminated thrombus formation can lead to cardiac infarction and organ damage consumption clotting factors causes internal bleeding and spread of infection multiple organ failure septic shock
45
what do interferons do?
interfere with viral replication
46
name 2 type I interferons, state the receptor that induces their expression and explain their purpose
IFNalpha IFNbeta induced by RIG1 and some TLRs when dsRNA sensed in cell induce a endoribonuclease that degrades viral RNA and protein kinase that P's eIF2 inhibiting protein transl
47
what do t-helper cells differentiate into
TH1 and TH2 cells
48
which cytokines do TH1 cells produce? what do TH1 cells do? what type of infections are they useful for?
produce: IL2, IFNgamma and TNF-alpha activate macrophages and induce B cells to make opsonizing antibodies (IgG) intracellular bacterial infections
49
which cytokines do TH2 cells produce? what do TH2 cells do?what type of infections are they useful for?
produce: IL4/5/6/10/13 (4 and 13 particularly important) induce B cells to make IgE helminths (big ol parasites)
50
name the 7 professional phagocytes
``` eosinophils neutrophils basophils mast cells dendritic cells monocytes macrophages ```
51
name the 4 polymorphonuclear granulocytes
neutrophils eosinophils basophils mast cells
52
eosinophils: location and concentration? receptors? defence against which pathogens? how do they kill pathogens? any extra deets?
small amount in the blood and also found under mucosal surfaces in connective tissue receptors for C3b, IgG, IgA, IgE defence against parasitic infections release toxic proteins/free radicals from granules synthesize cytokines and prostaglandins also have a role in allergy
53
basophils: location and concentration? receptors? defence against which pathogens? how do they kill pathogens? any extra deets?
low numbers in blood, more in tissue have high affinity receptor for IgE (FcεRI) as well as C3a, C5a granules contain histamine, ser-proteases and release interleukins defence against parasites, role in allergy
54
neutrophils: location and concentration? receptors? defence against which pathogens? how do they kill pathogens? any extra deets?
most common leukocyte in blood IL8 receptor v short lived unless moved into tissue (pus is essentially neutrophils) kill pathogens by: phagocytosis, release lysozyme and defensins, production ROI, production cytokines, NETs
55
mast cells: location and concentration? receptors? defence against which pathogens? how do they kill pathogens? any extra deets?
restricted to tissue - protect mucosal surfaces receptors for C3a, C5a and IgE release histamine and ser-proteases from granules sentinel cells defence against parasites, role in allergy
56
what is a key common feature of polymorphonuclear granulocytes in pathogen recognition
all express PRRs
57
name the mononuclear phagocytes
monocytes | macrophages (kupffer cells, microglia, lung alveolar macrophages, langerhans cells)
58
name the 3 APCs
dendritic cells macrophages B-cells
59
monocytes/macrophages: location and concentration? receptors? defence against which pathogens? how do they kill pathogens? any extra deets?
monocytes in blood --> macrophages in tissue most are classical subset: enter tissue and are inflammatory monocyte upon infection some are non-classical and roll along the endothelial wall phagocytic, kill by ROS/RNS also clear up cellular debris that could be harmful to body present extracellular pathogens on on MHCII
60
name the 6 types of phagocytic bactericidal mechanisms and give egs
acidification toxic oxygen-derived products (superoxide, hydrogen peroxide etc) toxic-nitrogen oxides (NO) antimicrobial peptides (cathelicidin) enzymes (lysozyme) competitors (lactoferrin - sequesters Fe2+ needed for bacterial survival - only in neutrophils)
61
describe the production of NO in cells
arginine + O2 ---> citrulline + NO | catalysed by iNOS2 (inducible nitric oxides synthase)
62
what is oxygen dependent killing and how does it work?
generation of superoxide anions by NADPH oxidase enzyme is activated by TLRs, chemotactic and some cytokine receptors generation of 'respiratory burst': transient increase in oxygen following phagocytosis due to activation of NADPH oxidase
63
how is inflammation resolved?
when neutrophils become apoptotic they release signals which inhibit further neutrophil infiltration. macrophages phagocytose apoptotic neutrophils
64
NK cells: location and concentration? receptors? defence against which pathogens? how do they kill pathogens? any extra deets?
found in blood recognition of cells by combination of stimulatory and inhibitory receptors stimulatory: natural cytotoxicity receptors inhibitory: killer immunoglobulin-like receptors (KIRs) eg MHCI kills cells by inserting cytoplasmic granules into plasma membrane by perforin. also use FasL and Fas and TRAIL and receptor NKs also use Antibody Dependent Cellular Cytotoxicity to kill infected (virus) and cancer cells (ADCC: abs bind pathogen, NK CD16 Fc receptors crosslink to ab --> apoptosis of pathogen) made my common lymphoid progenitor unlike all other innate cells)
65
dendritic cells: location and concentration? receptors? defence against which pathogens? how do they kill pathogens? any extra deets?
skin and lymphoid tissue activate naive T-cells in 2ndary lymphoid as well as differentiating T-helper into subpopulations take up foreign material by phagocytosis and show antigen to T-cells constitutively express high levels of MHCII
66
describe the stages of phagocytosis
bacterium binds surface phagocyte phagocytosis of pathogen by pseudopods invagination of phagocytic membrane traps pathogen in phagosome lysosome fuses with phagosome and deposits enzymes which cleave macromolecules and generate ROS/RNS release of microbial debris

MBB311 - Molecular Immunology (2 decks)

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