MICR221 EXAMINATION QUESTIONS WITH ALL CORRECT ANSWERS
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Module
MICR221
Institution
MICR221
MICR221 EXAMINATION QUESTIONS WITH ALL CORRECT ANSWERS
AB toxins - Answer-A has toxic enzymatic activity and B binds to receptors on host cells so A can be internalised by endocytosis
botulinum toxin - Answer-blocks release of acteylcholine from stimulatory motor neurons so no muscle contracti...
MICR221 EXAMINATION QUESTIONS
WITH ALL CORRECT ANSWERS
AB toxins - Answer-A has toxic enzymatic activity and B binds to receptors on host cells
so A can be internalised by endocytosis
botulinum toxin - Answer-blocks release of acteylcholine from stimulatory motor neurons
so no muscle contraction and flaccid paralysis
tetanus toxin - Answer-blocks release of glycine (stops acetylcholine release) from
inhibitory interneurons stimulating muscle contraction (uncontrolled)
how botulinum and tetanus toxins work - Answer-prevent exocytosis of vesicles
containing the neurotransmitter
V-SNARES on vesicles bind to T-SNARES (eg SNAP 25) on plasma membrane for
docking and fusion. toxins cleave V (some T) so stops
- different cells for the 2 different toxins so different effects
ActA - Answer-causes comet tail allowing it to move through cell
subverts human actin polymerisation (filaments) which causes motility through
"treadmilling" of actin subunits - off with ADP then on with ATP. this allows movement of
bacteria
ActA activates human Arp2/3 complex which stimulates actin polymerisation
innate immunity - Answer-rapid, low sensitivity eg phagocytosis - proteins are broken to
peptides and presented on MHC so T cells can recognise
adaptive immunity - Answer-slower initial but rapid memory and high specificity
B T and MHC
dendritic cell - Answer-most potent antigen presenting cell. breaks and presents
peptides on MHC and carries to lymph to T cells so they are activated and divide - many
pass through and specific activated.
CD4 T cells are activated
CD4 T cells - Answer-helper for CD8 which are cytotoxic lymphocyte (CTL) that kills
infected cells with virus/cancer
helper for B cells which produce plasma cells which produce antibodies
CTL - Answer-MHC have virus peptides, kill by stimulating organised programmed cell
death so pathogen gets killed
,antigen - Answer-anything recognised by the immune system
PRR - Answer-pattern recognition receptors recognise PAMPS and DAMPS
eg TLR and NLR are able to distinguish between types of pathogens allowing correct
immune response
TLR - Answer-ligand is bound, TLR dimerise which drags cytoplasmic tails leading to
recruitment of adaptor molecules. transcription factors are initiated so genes eg
inflammatory genes are expressed
endosome - Answer-has nucleic acid recognisers
NLR - Answer-in cytoplasm - recongises peptidoglycans. cleaves IKB so NFKB moves
to nucleus and is activated inducing transcription
how TLR and NLR improve immune system - Answer-greater pathogen clearance by
increasing cytokines and phagocytosis. increase capacity of APC and better T cell
stimulation and memory.
therefore vaccines have ligands that cause inflammation due to PRR, making adaptive
system better downstream
autophagy - Answer-tags intracellular pathogens with ubiquitin and phagosome
encircles and fuses with lysosome
MHC I - Answer-all nucleated cells, endogenous. 1 a chain non-covalently bound to
B2m. a chain binds peptide, but only small (9-10aa) due to conserved aa that weakly
interact with anchor residues on peptide
for CD8 T cells
polymorphic on a chain
MHC II - Answer-antigen presenting cells only, exogenous. a and b chains that both
bind peptides. longer peptides due to no conserved aa - extended open conformation
for CD4 T cells
polymorphic
dentritic cell exceptions for MHC II - Answer-express viral (endogenous) antigens on
MHC II by taking up dying cells and expressing on MHC II for CD4
dentritic cell exceptions for MHC I - Answer-express exogenous on MHC I due to cross
priming. phagolysosome leaks so antigens cytoplasmic and expressed on MHC I for
CD8 = cross priming
T cell recognition of MHC - Answer-recognises whole complex. MHC is unstable so
must be bound with self peptide - most MHC even when infected because dont need
much information
have chaperones when empty
, MHC I loading - Answer-foreign protein broken by proteosome, into ER by TAP.
chaperone holds, peptide added and chaperone leaves. expression on cell surface
MHC II loading - Answer-external protein taken up in phagolysosome, broken down.
MHC II with chaperone - chaperone is degraded - the peptide is loaded and expression
on cell surface
Ii protein - Answer-chaperone of MHC II - invariant chain. stabilises and prevents
premature loading of self. cleaved, but CLIP remains which is removed by HLA-DM and
replaced with antigenic peptide from endosome
DC and TC adhesion - Answer-interaction between MHC and TCR
CD8 and CD4 are weak stabilisers
stable adhesion between ICAM-1 on DC and LFA-1 on TC
signal 1 - Answer-many TCR being triggered when antigen/MHC binds
serial triggering - weak and fast interactions, so many TCR that are needed with 1 MHC
- efficient
signal 2 - Answer-co-stimualtion. DC only express CD80 when they see pathogens -
they bind to CD28 on T cells to activate T cells. CD80 activated by danger signals
recognised by toll like receptors. this prevents auto-immune.
some T cells are auto-reactive and have escaped tolerance induction in the thymus, so
if there is no CD80 then they are non-functional
what happens to T cells with no signal 2 - Answer-anergy (non responsive) or apoptosis
(killed)
IFNy - Answer-cytokine that makes macrophages cytotoxic for intracellular bacteria
Th1 - Answer-eg IFNy cytokines, for viruses and intracellular parasites
Th2 - Answer-eg IL-4 cytokines for extracellular bacteria and parasites. involved in
allergy (this and Th1 amounts programmed influenced by environment)
T cells - Answer-produced in bone marrow, move to blood, go to thymus where TCR
gene is rearranged by DNA splicing and screened.
recognise processed antigen peptides on variable a and b chains on binding site
T cells have different TCR (but same on same)
thymic selection of T cells - Answer-thymic stroma express MHC with self peptide. T
cells that cant bind are killed by neglect. if strong signal, T cells would cause
autoimmunity so are programmed to die if recognise self peptide, negative selection, if
moderate signal will survive - positive selection
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