BMSC334 EXAM QUESTIONS AND ANSWERS
100% CORRECT
common myeloid progenitors - ANSWER formed from hematopoietic stem cell and forms
innate immune cells
common lymphoid progenitors - ANSWER formed from hematopoietic stem cell and
forms lymphoid cells (b, t nk, ilc)
neutrophils - ANSWER granulocyte, most abundant phagocyte, first responder, enzyme
and antimicrobial substances
eosinophil/basophil - ANSWER granulocytes, rare, contribute to allergic reaction and kill
parasites too big to be phaged with enzymes and toxic proteins
mast cells - ANSWER mature in peripheral tissues, granules with inflammatory
mediators like proteases and histamine, present in allergic reactions
macrophages - ANSWER tissue residents, can originate from monocytes in blood,
phagocytes, produce inflammatory mediators, tissue repair, apc
innate lymphoid cells - ANSWER natural killer and interleukins, no specific antigen
receptor, alert other immune cells when activated, act quicker and respond to damps
pamps - ANSWER conserved repeated units of pathogen structures in the surface or
cytoplasm or nucleus eg. lps, CpG bacteria, viral ds rna
damps - ANSWER self molecules released from damaged, infected ot stress cells eg.
histones, dna, hmgb1, hsp
, classes of pattern recognition receptors - ANSWER TLRs, nucleotide oligomerization
domain and NOD-like receptors, retinoic acid inducible gene I like receptors, C type
lectin receptors
toll like receptors - ANSWER PRRs which can be cell surface bound for extracellular
pathogens or endosome bound for phagocytosed materials from pathogens, 10 in
humans
main tir/tlr adaptor molecules - ANSWER different ones for different tlrs, MyD88, TRIF,
TRAM, MAL
MyD88 adaptor TLR process - ANSWER dimerisation of TLR1+2 from lps binding,
cytoplasmic toll-interleukin receptor domains close, adaptor MyD88 recruited, recruits
IRAK1 and 4 which phosphorylate for activation, recruit TRAF6 and UBC13 ubiquitin
ligases, ubiquitin scaffold created on TRAF6, TAK1 recruited to it with adaptor TAB1/2,
TAK1 phos by IRAK to activate, recruits IKK which is phosphorylated by TAK1, induces
phos of IkkB which degrades and releases tf NFkB, released and migrates to nucleus for
transcription of pro-inflammatory cytokines like IL-6/TNFa and NLRP3
TAK1 - ANSWER induces NFkB tf or can stimulate MAPK which activates c-junction
terminal kinase and p38 for tf AP-1 and CREB
NOD like receptors - ANSWER sense bacteria and damage free in cytoplasm with card
domains
NODs signal transduction - ANSWER dimerisation after binding pamp or damp, brings
card domains together, recruit RIP2 kinase, ubiquitin ligase forms ub scaffold, more
proteins induce Nfkb activation
nlrp3 signalling - ANSWER transcriptional priming where TLRs 1/2 induce transcription
of NLRP3, non transcriptional priming where dec K+ due to membrane pore, ROS or
extracellular ATP dissociates chaperones on NLRP3, several of them oligomerise and
recruit adaptor proteins via CARD domains, forming a scaffold structure inducing
caspase cleavage to activate IL18/13
100% CORRECT
common myeloid progenitors - ANSWER formed from hematopoietic stem cell and forms
innate immune cells
common lymphoid progenitors - ANSWER formed from hematopoietic stem cell and
forms lymphoid cells (b, t nk, ilc)
neutrophils - ANSWER granulocyte, most abundant phagocyte, first responder, enzyme
and antimicrobial substances
eosinophil/basophil - ANSWER granulocytes, rare, contribute to allergic reaction and kill
parasites too big to be phaged with enzymes and toxic proteins
mast cells - ANSWER mature in peripheral tissues, granules with inflammatory
mediators like proteases and histamine, present in allergic reactions
macrophages - ANSWER tissue residents, can originate from monocytes in blood,
phagocytes, produce inflammatory mediators, tissue repair, apc
innate lymphoid cells - ANSWER natural killer and interleukins, no specific antigen
receptor, alert other immune cells when activated, act quicker and respond to damps
pamps - ANSWER conserved repeated units of pathogen structures in the surface or
cytoplasm or nucleus eg. lps, CpG bacteria, viral ds rna
damps - ANSWER self molecules released from damaged, infected ot stress cells eg.
histones, dna, hmgb1, hsp
, classes of pattern recognition receptors - ANSWER TLRs, nucleotide oligomerization
domain and NOD-like receptors, retinoic acid inducible gene I like receptors, C type
lectin receptors
toll like receptors - ANSWER PRRs which can be cell surface bound for extracellular
pathogens or endosome bound for phagocytosed materials from pathogens, 10 in
humans
main tir/tlr adaptor molecules - ANSWER different ones for different tlrs, MyD88, TRIF,
TRAM, MAL
MyD88 adaptor TLR process - ANSWER dimerisation of TLR1+2 from lps binding,
cytoplasmic toll-interleukin receptor domains close, adaptor MyD88 recruited, recruits
IRAK1 and 4 which phosphorylate for activation, recruit TRAF6 and UBC13 ubiquitin
ligases, ubiquitin scaffold created on TRAF6, TAK1 recruited to it with adaptor TAB1/2,
TAK1 phos by IRAK to activate, recruits IKK which is phosphorylated by TAK1, induces
phos of IkkB which degrades and releases tf NFkB, released and migrates to nucleus for
transcription of pro-inflammatory cytokines like IL-6/TNFa and NLRP3
TAK1 - ANSWER induces NFkB tf or can stimulate MAPK which activates c-junction
terminal kinase and p38 for tf AP-1 and CREB
NOD like receptors - ANSWER sense bacteria and damage free in cytoplasm with card
domains
NODs signal transduction - ANSWER dimerisation after binding pamp or damp, brings
card domains together, recruit RIP2 kinase, ubiquitin ligase forms ub scaffold, more
proteins induce Nfkb activation
nlrp3 signalling - ANSWER transcriptional priming where TLRs 1/2 induce transcription
of NLRP3, non transcriptional priming where dec K+ due to membrane pore, ROS or
extracellular ATP dissociates chaperones on NLRP3, several of them oligomerise and
recruit adaptor proteins via CARD domains, forming a scaffold structure inducing
caspase cleavage to activate IL18/13
