TEST BANK - MOLECULAR AND CELLULAR
IMMUNOLOGY, 10TH EDITION ALL CHAPTERS
WITH GRADED ANSWERS A+
What are some examples of covalent labelling strategies for t cells? -
ANSWER-Through intracellular protein binding: binds everything in the
cell with a certain group, transfer through generations, e.g. Maleimide
reaction labeling: binds thiol group at slightly acidic pH to form a
covalent bond, e.g. Succinimidyl ester labelling: binds primary amine
group at slightly basic pH, can have additional mechanisms to reduce
background fluorescence
there is some cross reactivity (infection with one pathogen alters the
susceptibility to infection with unrelated organisms in a lasting manner)
after primary exposure LPS (Lipopolysaccharide- and endotoxin from
outer membrane of gram - bacteria) which causes myeloid cells to make
cytokines- endotoxin tolerance builds up and lasts
macrophages can integrate environmental signals (including microbial
products) into their functional programs
mice defective in functional T and B lymphocytes can be protected
against re-infection with C. albicans (fungi) in a monocyte dependent
manner for up to 2 weeks after the primary infection
NK cells can proliferate (like t cells) a specific subset of cells for MCMV
(virus), this persists for several months
,What are red queen dynamics? - ANSWER-Hosts and pathogens
competing to evolve through selective pressures
e.g. host becomes resistant, pathogen must evolve to cause disease,
leads to complex/hypervirulent pathogens and complex immune
systems
What are antimicrobial peptides? - ANSWER-AMPs
in all living organisms
broad spectrum
secreted by cells
ancient immune system (just allows for competition between cells)
e.g. bacterocins (inhibit other bacteria, unusual AAs and PTMs)
e.g. alpha and beta defensins
e.g. lysozymes (in tear etc.)
How do AMPs work? - ANSWER-the majority exert their activity through
the interaction with membranes
some use cell wall inhibition (normally for fungi- either Glucan synthesis
inhibitors or Chitin inhibitors) and nucleic acid binding (mechanism
unknown)
some are thought to have an intracellular target
What happens when AMPs come into contact with membranes? -
ANSWER-an induce the formation of secondary structures, such as α-
helices, β-sheets, or a mixture of both, that are critical to antimicrobial
activity
usually work to form pores via one of three models:
,Barrel-stave model- peptides aggregate and form barrel-shaped pores in
the membranes
Carpet model- peptides accumulate on the membrane in a carpet-like
manner, attracted by electrostatic interactions
Toroidal pore model- peptides insert into the membranes, forming pores
and tilting the lipid layers in the fashion of a toroidal hole (donut shaped)
What are pattern recognition receptors? - ANSWER-PRRs
eukaryotic
induce inflammation, start the immune response
recognise general pathogenic ligands (pathogen associated molecular
patterns (PAMPs))
can be toll-like (recognise PAMPs) or NOD-like (intracellular)
What is nucleic acid recognition? - ANSWER-simplest form of immune
mechanism
multiple types via convergent evolution
use of genetic material for immunity
e.g. RNAi (monophyletic and eukaryotic), restriction enzymes
(polyphyletic), CRISPR-Cas (bacteria)
What is the complement system? - ANSWER-unclear origins
plasma proteins that react with each other to opsonise pathogens and
activate inflammation
a global regulator of immunity and tissue homeostasis
found in animalia
, 3 pathways: classical (antigen:antibody), lectin (recognises
carbohydrates), alternative (recognised pathogen surfaces)
What are reactive oxygen species? - ANSWER-ROS
highly reactive molecules
damage DNA, oxidise lipids and proteins
can be a byproduct of metabolism but can also be synthesised by
bacterial prokaryotes and eukaryotes for defence
archaea can defend against but not create them
How is apoptosis used in the immune system? - ANSWER-unclear origin
eukaryotic and multicellular only
used to prevent disease spread triggered by DNA damage, virus,
mitochondrial signals, receptor activation etc.
What are the physical and physiological parts of the innate immune
system? - ANSWER-epithelia and endothelia sealed by tight junctions
external epithelium keratinised (strong and waterproof), allows for
picked up pathogens to be shed with dead skin cells
internal flow maintained by peristalsis, cilia and fluid- this moves
pathogens along
physiological: stomach pH, body temp
Ecological: niche deprivation by gut flora
Chemical: defensins- alpha in GI and beta in skin and lungs)
What is restriction modification? - ANSWER-restriction enzymes cut
dsDNA (double strand) at specific sequences
then the DNA can be further degraded
IMMUNOLOGY, 10TH EDITION ALL CHAPTERS
WITH GRADED ANSWERS A+
What are some examples of covalent labelling strategies for t cells? -
ANSWER-Through intracellular protein binding: binds everything in the
cell with a certain group, transfer through generations, e.g. Maleimide
reaction labeling: binds thiol group at slightly acidic pH to form a
covalent bond, e.g. Succinimidyl ester labelling: binds primary amine
group at slightly basic pH, can have additional mechanisms to reduce
background fluorescence
there is some cross reactivity (infection with one pathogen alters the
susceptibility to infection with unrelated organisms in a lasting manner)
after primary exposure LPS (Lipopolysaccharide- and endotoxin from
outer membrane of gram - bacteria) which causes myeloid cells to make
cytokines- endotoxin tolerance builds up and lasts
macrophages can integrate environmental signals (including microbial
products) into their functional programs
mice defective in functional T and B lymphocytes can be protected
against re-infection with C. albicans (fungi) in a monocyte dependent
manner for up to 2 weeks after the primary infection
NK cells can proliferate (like t cells) a specific subset of cells for MCMV
(virus), this persists for several months
,What are red queen dynamics? - ANSWER-Hosts and pathogens
competing to evolve through selective pressures
e.g. host becomes resistant, pathogen must evolve to cause disease,
leads to complex/hypervirulent pathogens and complex immune
systems
What are antimicrobial peptides? - ANSWER-AMPs
in all living organisms
broad spectrum
secreted by cells
ancient immune system (just allows for competition between cells)
e.g. bacterocins (inhibit other bacteria, unusual AAs and PTMs)
e.g. alpha and beta defensins
e.g. lysozymes (in tear etc.)
How do AMPs work? - ANSWER-the majority exert their activity through
the interaction with membranes
some use cell wall inhibition (normally for fungi- either Glucan synthesis
inhibitors or Chitin inhibitors) and nucleic acid binding (mechanism
unknown)
some are thought to have an intracellular target
What happens when AMPs come into contact with membranes? -
ANSWER-an induce the formation of secondary structures, such as α-
helices, β-sheets, or a mixture of both, that are critical to antimicrobial
activity
usually work to form pores via one of three models:
,Barrel-stave model- peptides aggregate and form barrel-shaped pores in
the membranes
Carpet model- peptides accumulate on the membrane in a carpet-like
manner, attracted by electrostatic interactions
Toroidal pore model- peptides insert into the membranes, forming pores
and tilting the lipid layers in the fashion of a toroidal hole (donut shaped)
What are pattern recognition receptors? - ANSWER-PRRs
eukaryotic
induce inflammation, start the immune response
recognise general pathogenic ligands (pathogen associated molecular
patterns (PAMPs))
can be toll-like (recognise PAMPs) or NOD-like (intracellular)
What is nucleic acid recognition? - ANSWER-simplest form of immune
mechanism
multiple types via convergent evolution
use of genetic material for immunity
e.g. RNAi (monophyletic and eukaryotic), restriction enzymes
(polyphyletic), CRISPR-Cas (bacteria)
What is the complement system? - ANSWER-unclear origins
plasma proteins that react with each other to opsonise pathogens and
activate inflammation
a global regulator of immunity and tissue homeostasis
found in animalia
, 3 pathways: classical (antigen:antibody), lectin (recognises
carbohydrates), alternative (recognised pathogen surfaces)
What are reactive oxygen species? - ANSWER-ROS
highly reactive molecules
damage DNA, oxidise lipids and proteins
can be a byproduct of metabolism but can also be synthesised by
bacterial prokaryotes and eukaryotes for defence
archaea can defend against but not create them
How is apoptosis used in the immune system? - ANSWER-unclear origin
eukaryotic and multicellular only
used to prevent disease spread triggered by DNA damage, virus,
mitochondrial signals, receptor activation etc.
What are the physical and physiological parts of the innate immune
system? - ANSWER-epithelia and endothelia sealed by tight junctions
external epithelium keratinised (strong and waterproof), allows for
picked up pathogens to be shed with dead skin cells
internal flow maintained by peristalsis, cilia and fluid- this moves
pathogens along
physiological: stomach pH, body temp
Ecological: niche deprivation by gut flora
Chemical: defensins- alpha in GI and beta in skin and lungs)
What is restriction modification? - ANSWER-restriction enzymes cut
dsDNA (double strand) at specific sequences
then the DNA can be further degraded
