Review Flashcards
cell wall in gram pos
peptidglycan layer outside cell membrane
what add’l feature present in gram pos and neg
capsule
what does capsule do
makes bacteria difficult to phagocytes to deal with unless it can be opsonized
compare and contrast gram neg and gram pos bac
ppt
what Ig do we need to opsinize capsule
IgG
difference b/w cell wall of gram pos and gram neg
thickness
what do we use to do use to differentiate if its gram pos or gram neg
gram stain
gram pos vs gram neg cell wall
gram pos 10x thicker
gram stain does what with gram pos
it’s trapped - crystal violet die is trapped so stained purple “violet”
gram pos will stain
blue (purple)
gram pos associated with the cell wall
teichoic acid & lipoteichoic acid
what two things are unique to gram pos
teichoic acid
lipoteichoic acid
describe gram stain and list the steps
to see if bacteria is pos or neg. fixation crystal violet iodine treatment decolorization counter stain safranin
LPS is part of gram pos or neg
gram neg
what TLR to detect LPS
TLR4
what is the toxic component of LPS
Lipid A component
four main mechanisms stuff can be transffered b/w bac
transposition
transformation
conjugation
transduction
transposition
transposons
the movement of small pieces of DNA called transposons to different locations in the genome and between plasmids. These are sometimes called “jumping genes.”
transformation
ability of bacterium to take up DNA from enviornment and stabilize by recombination into own chrom
“uptake of naked DNA”
conjugation
transfer of plasma DNA following contact or transfer of bacterial chromosomal genes if it recombines, then can transfer bacterial chromosomal genes that lie closest to the insertion point of the plasmid
the transfer of DNA through cell-to-cell contact
transduction
exchange of genetic info mediated by viruses that infect bac
the transfer of genetic information via bacterial viruses (phages).
two main mechanisms of transduction
generalized
specialized
generalized transduction what cycle
lytic cycle
specialized transdicution mediated by
lysogenic or temperate phages
lysogenic phages do what
integrate their DNA into DNA of bacerial cell and can remain there for life of bacteria as prophage
during latent stage describe phage DNA
not silent
if bacterium becomes friend prophage can be
reactivated
mistsake that leads to specialized transduction
sometimes it doesn’t come out exactly the right way - sometimes it can be half infectious half not.
review pg 6 and understand - review ppts if don’t understand
pg 6
F+ by F- cross what are you doing
transferring conjugal plasmid
male cell has
f pillus
single strand cleaveage at
origin of transfer
conjugation and transfer you need
male and female
at the end of conjugateion both cells
are donor cells
all that is transferred in conjugation transfer are
genes on plasmid
main difference b/w F+ F- and Hfr
all that is transffered on F+ F- is plasmid
Hfr cross where does it always happen
origin of tranfer
Hfr cross you will never transfer
genes encoding F pillus
why won’t you ttansfer genes for f pillus at Hfr cross
they are the very end and they don’t get transffered
to be able to transfer the f pillus you have to transfer what for Hfr
entire DNA for Hfr
what is end result of Hfr
recipient always F-
it may aquire bacterial chromosomal genes from donor
what does a virus need to have
genome
what kind of genome can virus have
DNA or RNA
DNA genomes in virus can be
linear or circular
single-stranded or double stranded
RNA genome can be
linear or segmented
single stranded or double stranded
infleunza is example of virus with
segmented genome
positive sense RNA is
like mRNA
negative sense RNA pripor to translation
have to be converted to positive sense
positive sense RNA prior to translation
cn just be translated, its like mRNA
ambisense means
+ at one end - at the other end
positive sense RNA viruses do not need
RNA dep RNA pol
but they encode it
two structures possible for capsid
helical or icosahedral
all that naked virus is
capsid genome
enveloped viruses have what on outiside
lipid bilayer - from host cell when they budded
how do virus get envlope
from budding from host cell
what is envelope for virus
lipid bilayer
what are the targets for neutralizing antiodies for viruses
peplomers
if virus needs something host cell cannot provide then
virus has to bring it with it
examples of packaged enzymes for virus
replicases
proteases
structural proteins
part of the virion itself
non-structural proteins
not part of virion
virally encoded enzymes are not always packaged in
virion
if something is required to get to mRNA then they have to be what in virus
packaged
if somethign is needed after mRNA stage for virus replication they have to be what in virus
encoded doesn’t need to be packaged
naked virus is released by
lysis
enveloped virus are released by
budding
what steps do all viruses need to go through intheir life cycle
adherence penetration replication assembly release
HIV fuses at what pH
neutral
influenza virus fuses at what pH
acidic
what is pH independent fusion
neutral pH fusion
what is pH dependent fusion
acidic pH fusion
b/c influenza virus will only form at acidic pH cannot form
syncytia
HIV and other things that fuse at neutral pH can form
syncytia
review replication strategies of virsues
pg 13
site of replication dictates what dna virus
has to bring with it
vast majority of dna viruses replicate in
nucleus
vast majority of rna viruses replicate in
cytoplasm
rna virus replication exception
orthomyxoviruses replicate in nucleus
dna virus replication exception
poxviruses replicate in cytoplasm
depending on the cell that dna virus replicates is a replicating cell or quiescent determiens
if they need to bring polymerase with them
quiescent cells don’t have what
polymerase b/c they won’t be replicating
retroviruses and hepadnaviruses replicate where
both - have stage in cytoplasm and nucleus
can get formation of what for viruses that replicate in nucleus
intranuclear inclusion bodies
if enzyme is required for production of mRNA and cell cannot provide it must be
pakcaged
if enzyme is not needed to get to mRNA but is required in replication and host cell cannot provide it must be
encoded, but doesn’t need to be packaged
chitin rechognized by
TLR2
LPS recongized by
TLR4
flagellin recognized by
TLR5
beta-glucan recognized by
dectin-1
viral nucleic acid intracellular PRR
TLR3, 7, RIG-I
bacterial DNA intracellular PRR
TLR9
pRR is a
pattern recogniztion receptor
lipids etc of intracellular bacteria PRR
NOD1 NOD2
mannosylated molecules can be recongized by
MBL & Ficolins & lectin
antibody bound to pathogen can be recognized by
C1q
need how many IgG for C1q to bridge gap
2 - only need 1 for IgM
when c reactive protein binds to lipid on surface of bacteria it allows
c1q to bind directly to reactive protein
review the complement video
:)
for direct activation of pathogen surface is what pathway
alternative
just reivew my compleemtn chart and the video
.
low levels of C2 and C4 predispose you to?
immune complex disease
defect in C1-INH what disease
HAE
CD45 is
DAF
DAF stands for
decay accelerating factor
C3b is
opxinin
C3b allow
phagocytes to bind and enhances the ability of phagocyte to take up bacterium and destroy
what is the highest concentration in complement
C3
C5a is
chemoattractant
C3a is
chemoattractant
C3a and C5a are chemoattractant and they also attract
mast cells
what is first part of mac formation
C5b
an anything prevent formation of MAC on our own cells?
CD59
CD59 is also known as
protectin
protectin does what
stops complement from forming on our own cells
low levles of C3 susceptible to
recurrent bactieral infections, esp with encapsulated bacteria
no MAC, suscpetible to
nisseria infections
when is complement activated
following binding of initiators to pathogen surfaces
C1q is part of which complement ptahway
classical
MBL/ficolins pat of which compelemtn apthway
lectin
C3b is part of what complement pathway
alternative
MAC causes lysis of what two things
gram neg
enveloped
what attacks gram pos bacteria
lysozyme
c3b and c4b are
opsinins
c5 and c3 a are
leukocyte chemoattractants
c5a and c3a increase
vascular premeability, complement proteins, and bradykinin
bradykinin mediates
pain
c5a and c3a induce
mast cell activation and degranulation
binding of PAMp to mast cell PRR can induce
degranulation
mediators relased by mast cells
histamine
TNF alpha
IL-1
IL-8
what does TNF alpha and IL-1 do
increase vascular permeability
increase adheion molecules on vascular endothelial cells (allows phagocytes to bring themselves to a halt)
most potent chemoattractant for neutrophils
IL–8
IL-8 is
leukocyrte chemoattractant
IL-12 activates
NK cells
and signal 3 for differentation of CD4 into Th1 cells
TNF alpha, IL-1, and IL-6 induce
acute phase response
what is always first cell at site of inflammation
neutrophils
what is most abundant leukocyte
neutrophils (also the fastest!)
draw out leukocyte extravasation from tissues
pg 23
dissease cD18 is defective
LAD1
disease CD 15 defective?
LAD II
draw out steps of phagocytosis
pg 24
gram neg bac will stain
pink
LPS (lipopolysacchardie) is also called
endotoxin
besides TLR4 what detects presence of LPS
LPS binding protein & CD14
main killing mechanism of neutrophils
oxidative killing
oxidative killing mechanism dependent on what complex
NADH oxidase
oxidative pathway of killing is induced by
exposure to chemoattractants
besides oxidative killing pathway what can neutrophils do
non-oxidative killing
what are examples of enzymes in non-oxidative killing pathway
elastase
cathespins/orher proteinases
colalgenase
lactoferrin
lack of oxidative pathway is not sufficient, how do we know
chronic granulomas disease
during inflammation greatly increase prduction of ____ from bone marrow
neutrophils
after neutrophil what is next cell to enter site of infection
monocyte
most of neutrophils that fight site of infection will
die :(
macrophaegs come in after neutrophils to
clean up the pathogen and the dead and dying netrophils
what is netosis
explosive death of netruphils where they expell their proteins
what does netosis expell
histones, degradative enzymes, proteinase 3, especially PEPTIDYL ARGININ DEIMINIASE (PAD)
NETs stands for
neutrophil exraclular Traps
nets function as
traps for bacteria - make the bacteria more easily to deal with by monocytes (macrophages)
when monocytes arrive at site of infection they differentiate into
macrophaegs
notecard pg 29
29
when dendritic cells acquire antigen and they are migrating to lymph node they are
processing antigen so they are ready to present antigen to t cell when they get to lymph
explain exogenous pathway
pg 31
expalin endogenous pathway
pg 31
endogenous pathway
processing antigen made inside cell
exogenous pathway
processing antigen take up from outside cell
acidic vesicles are responsibel for
processing of antigen into peptides
endosome becomes progressivly
acidified
drop in PH activates
the things that will degrade antigens into short peptides
which MHC for exogenous pathway
MHC class II
what is antibody good at
good at getting what is outside of cells
restrict activation of CD4 t cells to peptides derviced from amterial that comes in from
outside of cell -b /c it will help b cells make antibody against the material
t cell epitope and b cell epitopes have to be
linked
to help b cell make antibody against extraclelular antigen
must be linked to t cell
invariant chain describe function
block class II from binding peptides from endogenous material binds to MHC II, blocks binding groove and stops things that shoudl bind to MHC I to bind to MHC II
redirects class II to where the peptides are - endosomal comparemtnt
what is CLIP
what is left in MHC II binding groove after it has been cleaved
HLC-DM catalyzes change of
CLIP for peptide
immunoproteasome
cleaves proteins into short peptides
in ER peptides that are gnerated bby proteasome can bind to MHC I then
disassociates from calenxin and geos to calreticulin
what does calnexin do
holds MHC I until beta2M arrives
draw out endogenous pathway
check iwth old notes to get right
draw outexogenous pathway
check with old notes to get it right pg 31
eptiopes for b cells tend to be
hydrophilic
peptides recognized by t cells tend to be
hydrophobic
MHC required for b cells
no
mhc required for t cells
yes
10:44
put in the proper slide it’s weird in my power point
t cell and be cells arise from common progenitor cell
draw out/explain the maturation of t cell and b cell
pg 33
heavy chain locus made up of
VDJ
always which locus to rearrange first
heavy chain
after heavy chain has passed test for functionality (tested by surgoate light chain ) then you will
rearrange kappa or lambda light chain (humans use kappa more)
process that heavy chain and light chain brought otgether
somatic recombination
first locus to rearrange always
heavy chain
light chain rearrangement governed by what rule
12 23 rule
following rearrangement for light chain you bring what together
VJ
first rearrangement in heavy chain
DJ
second rearrangment in heavy chain
DJ then VDJ
after chain rearrangment, list steps
transcription primary RNA trancript RNA pslicing mRNA translation H or L protein
what are enzymes responsible for rearrangment of chains
RAG1
RAG2
Tdt
artemis (omenn)
assumign we arrange functional beta chain we are almost certain to
rearrange functional alpha chain
how many chances to rearrange alpha chain
lots
first rearrangment of beta chain lcous
DJ then VDJ
rearrangment at alpha chain locus
VJ
CDR3 not encoded in
germline - it’s generated in recombination process
CDR3 is most variable b/c
imprecision involved in joining
n nucleotide addition by
TdT
first rearragnemtn in b cell
D to J in heavy chain
first rearrangment for t cell
beta chain D to J
after heavy chain rearrangemnt check if its functional by
pairing with surrogate light chain (b cell) surrogate alpha cell (thymocyte)
list steps for b cell rearrangemnt
pg 45/44 and go to previous ppts to get corect
list steps for t cell rearrangemnt
pg 45/44 and go to previous ppts
beta chain has to be able to pair with what to survive
surrogate light chain
how many chances to rearrange beta chain
4 - two on each chromosome
once you have heavy chain that works what do you do
allelic exclusion & proliferation - you have one that works keep it and make a lot of it
follwoign proliferation of pre b or t cell
start rearranging nex thting, so alpha in thymocyte and l chain in B cell
pre t cell needs to start expressing what after they rearrange the alph chain and stop expressing pre-T alpha
start expressing CD4 and CD8
will keep the one that work best and then get rid of the other
surrogate chain is test of function for
first chain rearranged
test ofr light chain is
heavy chain i nterms of b cells
see if it pairs with beta chain for TCR
co-expression ofi IgM and IgD happens at what level
RNA - alternative splicing
ability to secrete Ig is
RNA - alternativ splicing
irrevirsible changes in b cell happen at
DNA level
what happens in b cell that is irreversible change
pg 46
once you switch from making igM to IgG you can’t
go back to making IgM b/c you’ve deleted the new gene segment from chromosome, but you cant switch to something downstream like IgA
1st checkpoint for b and t cell
pre receptor
preBCR or preTCR
second checkpoint in t and b cell development
second chain so light chain or alpha chain
after 2nd checkpoint allows cells ot undergo
election
when common lymphoid progenitor enter thymus and have notch ligand interaction they become first definable stage during t cell development and they do not express
CD4 or CD8
double negative
signal for expression of CD4 and CD8 comes through
pre TCR signal
following beta rearrangment and expresion f PreTCR you will start to express what on surface
CD4 and CD8
after CD4 and CD8 will start to rearrange
alpha chain
double positive cells will go onto
selection
first part of selection happens where
cortex of thymus on surface of cortical epithelial cells
cortical epithelial cells express
MHC I and MhC II
if not interaction b/w MHC I and MHC II w/ t cell
t cell will die
if TCR binds with high affinity to MHC presenting thymic peptide, what happens
t cell death
outcome we want with TCR binding to thymic peptide
low affinity to MHC I or MHC II
when TCR binds with low affinity it will
survive
if TCR interacts with class I then
it wil be CD8
if TCR interacts with class II then
it will be CD4
CD3 signal maintains expression of what if TCR binds to MHC II
CD8 and loses expression fo CD4
T cells arriv in medulla as
single positive - CD4 or CD8 not both
if TCR recognized CD1d moelcule prsenting lipid r glycolipid they will
leave at that stage as double positive NKT cells
most important negative selection for t cells location
medulla or boundary of medulla
cells that mediste negativeselection in medulla that is most important negative selection
AIRE
what does aire do
expresses celsl found elsewhere in the body so you can get rid of self reactive T cells
CD4 t cells if there is intermediate affinity b/w TCR and mHC peptide complex then what happens
turns on expression of Foxp3 and becomes Treg
what TF to become Treg
FOxp3
Tregs that develop in thymus and in periphery are important for
silencing autoreactive t clls
what is first pre or pro b
pro then pre b
if BCR binds to self proteins then
there is opportunity to rescue BCR from autoreactivity by replacing light chain rearrangment with alternative light chainr earrangment
how many chags to reararnge b cell light chain
lots!
immature b cell stage can reactivate what
recombinase to try and replace the light chain rearrangement with alternative light chain to have it not be autoreactive or until you’ve used up all the J gene segments
if b cell has used up all j segments and still autoreactive
death
draw out an antibody
pg 50
where is Fab on antibod
pg 50
ends that interact with antigen
antigen binding site - include hypervariabl region
Fc portion harbors
effector functions
what is responsibel for acivating classical pathway of complement and what Fc receptor the IG can bind to
Fc portion
Fab contains
variable region of heavy and light chain and first constant of heavy and only constant of light chain
CDR1 and CDR2 are
encoded in VG segments in heavy and light chain
CDR3 is generated through
joining
constant domain in Fc portion determine
biological function
most abundant Ig
IgG
first antibody you wil make is
IgM
during primary response you will switch to what isotype usually
IgG
important function of IgG is
passive immunization of neonate due to placental transfer
IgM structure
pentamer
most Ig are what structure
monomer
in circulation IgM is what structure
penatmer
on cell surface IgM is what structure
monomer
first Ig made during fetal development
IgM
IgD structure
monomer
IgD is found where
membrane bound on mature B cells
IgA in ciruclation is what structure
monomer
majority of IgA secreted as what in mucosa
dimer
what holds two IgA together
J chain (I think?)
lowerst Ig
IgE
majority of IgE is
boudn to Fc epsiolon receptor on mast cells or basophils
IgE important in what kind of response
allergic response and involves responses against parasites
IgE structure
monomer
mu heavy chain is what Ig
IgM
what is most efficient isotype to activate complement
IgM
why is IgM so good at activating complement
pentamer so only need one
only Ig to cross placenta
IgG
monomeric IgM binds with what affinity
low
pentameric IgM affinty and avidity
low affinity but high avidity b/c there are so many of them
IgG subclasses
1,2,3,4
gamma is what Ig
IgG
what IgG subclass is greatest amount
IgG1 (so IgG4 is lowest)
once b cell switches to IgG BCR is
IgG
best IgG sublcasses for complement activation
IgG1 and IgG3
IgG is very important for
opsonization
what IgG subclass poorest at crossing placenta
IgG2
tapasin facilitates
putting peptides into MHC b/w α1 and α2
explain MHC Class I pathway
Virus enter cell, replicates, get proteins that are made in cytosol, so the protein is made in our own cells cytosol, proteasome, chops the protein made by viral mRNA into pieces, peptide piece brought into ER, LHA class I with peptides will be expressed on surface
explain MHC class II pathway
Big picture: infection, exracellular. Probalby bac. Take it in via endocytic vesicle, chop into pieces, miss with lysosome, bring MHC II and combine the two vesicles (one with pieces with MHC II) and express it on the outside. The origin of peptide was extracellular infection
most abundant Ig we have not in serum
IgA but not in serum (but overall it is the most abundant we have)
most important mucosal defense
IgA
IgA subclasses
IgA 1 & 2
what holds IgA dimer together
J chain
what holds pentimer of IgM together
J chain
heavy chain of IgA is
alpha 1 or alpha 2
IgA1 can activate complement by what pathway
alternative & lectin
IgA secreted across epithelial cells following binding of
pIgR via J chain
heavy chain of IgE
epsilon
minority of Ig in serum
IgE
can IgE activate complement
no
IgE can bind to high affinity Fcepsiolon receptors in absence of
antigen binding - which is how mast cells become senstized during hypersenstivity responses
majority of IgE is boudn to
high affinity (Fcepsiolon) on mast cells and basophils and eosinophils
IgE major role
parasitic infections and also associated with allergy
what HSR is IGE associated with
HSR1
heavy chain of IgD
delta
can IgD activate complement
no
main role of IgD
b cell receptor on mature naive b cells
what kind of splicing leads to expression of IgD
RNA
once t and b cells develop they go to
secondary lymph
t cells go to where in lymph node
paracortex
b cells go to where in lymph node
follicles
antigen taken to lymph and can be taken what two ways
carried actively by dendritic cells
free in lymph fluid
when dendritic cells take antigen to lymp h where do they take
paracortex
when freel ymph carries antigen to lymph where does it take it
follicle & paracortex
b cell zone and t cell zone are largely non-overlapping but you do find some t celsl in b zone area, which t cells
folliclular helper t cells
if dendritic cell doesn’t find t cell to respond to it then it will
DIE
if dendritic cell finds mhc to reognize what it is holding then it will
proliferate
following signal 1 and 2 to t cell will get
clonal proliferation
what IL drives proliferation of t cells
IL-2
steps in adaptive t cell mediated immune response
Clonal selection - binding of APC by an antigen specific T cell, primarily in peripheral lymph organs
Signal 1 - APCs present peptide-MHC(Ag/MHC) to TCR on CD4+ T cells (T helper (Th) cells)
Signal 2 - APCs present co-stimulatory molecules to CD28 on T cell leading to IL-2 production and IL-2R expression
Clonal expansion - T cells are now receptive to autocrine (CD4+ T) and paracrine (CD8 T) stimulation by IL-2 leading to proliferation
Differentiation - T cells respond to cytokines to become effector and/or memory T cells
what IL allows clonal expansion
IL02
clonal expansion of CD4+ t cells is
autocrine
clonal expansion of CD8 t cells is
paracrine
after clonal expansino phase undifferentiated t cells are now receptive to signals that will
bias their differentiation into one of the CD subset
Th0 is
uncommitted CD4 t cell
cytokines bias to T-bet TF
IL-12 & IFN gamma
T-bet promote differentiation into
Th1 cells
Th1 cells secrete
IFN gamma
IL-4 will turn on expression of what TF
GATA-3
GATA-3 will differentiate into
Th2
Th2 promote what immunity
humoral immunity
Th1 promote what immunity
cel-mediated
GATA-3 and Th2 esecrete
IL-4
TGF beta will turn on expression of what TF
Foxp3
Foxp3 will cause t cell to differentitate into
Treg
Treg secrets
TGF beta and IL-10
TGF beta and IL-6 turn on expression of what TF
RORgammat
most pro-inflammatory subset
Th17
RORgammat cuase t cell to differentiate into
Th17
role of th17
pro-inflammatory
Th17 secrete
IL-17
key role of IL-2
Growth factor for Th0 cells and Th1 cells
Induces clonal proliferation Th0 cells
Secreted by Th0 cells and Th1 cells
key role of IL-12
Induces differentiation of Th0 cells into Th1 cells
Produced by APC
key role of IFN gamma
Induces differentiation of Th0 cells into Th1 cells
Inhibits proliferation of Th2 cells
Important for cell-mediated immunity (activates macrophages)
Produced by Th1 cells
key role of IL-4
Growth factor for Th2 cells Inhibits proliferation of Th1 cells Growth factor for B cells Important for humoral immunity (stimulates antibody production) Produced by Th2 cells
how does Th1 cell activate macrophage
CD40L bind to CD40
IFN gamma bind to IFN gamma receptor
Th1 how do they help for virus infections
they induce CTL differentiation (killer cells)
if Th1 cell recognizes same antigen as a CTL cell then
Th1 will secrete IL-2 and then CTL be activated, now it can kill and will secrete perforin and granzymes
key cytokine for promoting synthesis of perofrin and granzymes
IL-2
how do you measure CTL or NK cell killing activity? what assay?
chromium release assay (chromium 51, following killing it will be released and measure the amoutn released which indicateds the amount of killing)
review pg 69
69
follwing activation t ell will express
CD40L but only briefly
centorblasts
t cells that are actively rearranging VDJ
extracellular pathogens need
high titer antibody response
review pg 70
70
review pg 71
Know cell type in innate response and adaptive response what will control the infection and what is inappropriate and would cause severe disease
humoral immunity is
antibodies
cell mediated
does not involve antibodies
dipetheria
protein based subunit vaccine
go to vaccine ppt we need to know different vaccines
you can do it
MMR vaccine
measles, mumps, rubella
type of vaccine MMR
live attenuated
example natural passive immunization
transcplacental IgG
purpose of subunit conjugate polysaccharide vaccines
generate t dependent response against polysacchardie
encapsulated bacteria surface is to polysacharide, cannot deal with them unless they are opsinized, so need IgG. isotype switching will not happen without t cell help, and t cells will not recognize polysaccharides
active natural immunization
infectino
active artifical imunization
vaccination
isotype switching will not happen without
t cel lhelp
name four live/attenuated vaccines
MMR
varicella
influenza
rotavirus
name 2 inactivated/killed vaccines
polio (IPV)
hep A
if you give someone inactivated poliovirus vaccine how will that be handeled by immune system after being taken up by dendritic cells
exogenous pathway b/c it’s inactivated so cross presentation pathway isn’t active
MHC II via exogenous pathway to CD4 t cells
name a toxoid/inactivated toxin vaccine
dipehteria, tetanus
name six subunit/conjugate vaccine
hep b influzna (injection) Hib pertussis pneumonococcal meningococcal
review pg 74
74
fastest type of rejection
pre-existing antibodies, hyperacute rejection
antibodies that mediate hyperactue rejection are
easy to screen for
most common form of graft rejection
acute rejection
acute rejection usually mediated by
recipient t cells
how long does acute rejection usually take
7-10 days
if transplant rejected by acute rejection may need second transplant, if the second shared some MHC mismatches that were from the first one, then can get what direction
accelerated
describe accelerated rejection of graft
memory response
how many days for accelerated rejection
a few days
what is cause of accelerated rejection of graft
reactivation (memory) pf sensitized t cells
what is cause of graft versus host disease
Primary activation of donor T cells in transplanted bone marrow
how long does GVHD take
days-weeks, minimum 7-10 days
what cells are most important in preventing outgrowth of tumors
CD8+ CTL mediated lysis
CD4+ helper role
NK cell killing
Macrophages
if macrophages infiltrate a solid tumor then they will turn into
immunosuppressant cells :(
TSA is
antigen that is expressed by tumor cell but not any other cell regardless of stage of differentiation
mutations
TSA stands for
tumor specific antigen
E6 and E7 proteins of HPV in cervical cancer cells is that TSA or TAA
TSA
TAA is
over-expressed normal proteins
checmical/radiation induced cancers it at TSA or TAA
TS
review pg 78
78
if it is type IV the antibody is not pathogenic b/c
it is not humoral, it is cell mediated
revie pg 79
79
B27 strongly associated with
ankylosing spondylitis
LADI is due to what deficiency
CD18
LAD II due to what deficiency
CD15
CGH due to what deficiency
NADPH oxidase
susceptibility fo individuals with low levels of C3 and components of alternative pathway
encapsulated bacteria
CHS is due to what deficiency
LYST
C1, C2, C4 deficiencies predispose pt to
immune complex disease
MAC deficiency (C5-9) susceptilbity to
neisseria infections
mutations in PIGA gene (CD55 & CD59) gives rise to what disease
paroxysmal nocturnal hemoglobinuria
C1-INH gives rise to what disease
Hereditary Angioedema (HAE)
XLA genotype
Btk mutated
XLA phenotype
no B cells
X linked hyper IgM genotype
CD40L
X linked hyper IgM phenotyep
no class witching, no GC
AR hyper IgM genotype
AID deficiency
AR hyper IgM phenotype
no class switching but giant germinal centers
selective IgA deficiency genotype
unknown
selective IgA phenotype
anti-IgA (especialky of IgE isotype)
CVID genotype
various defects
CVID phenotype
adolsescent, later onset
selective IgG subclass deficiency genotype
defect uknown
selective IgG sublcass def. phenotype
discvoered inadvertently
clinical presentation of someone with omenn syndrome
SCID with eosinophilia
T cells that get out are useless
DiGeroge syndrome phenotype
no thymus
thymic hypoplasia sometimes aplasia
X linked proliferative syndrome clinical presentation?
cannot control viral infections, esp EBV
fulminant EBV infection
Wiskott aldrich syndrome presentation?
classic triad:
ecezma
ataxia telangiectasia associated with
IgA deficiency
difficulty walking
increase in serum levels of alpha beta protein
multiple myeloma how would it present
pg 85 notecard
notecard pg 86
86
88
notecard pg 88
notecard pg 89-94
yay
describe conjjgate polysaccharide vaccine
have to link polysaccharide to peptide so b cell take it and be able to present to t celland can get cd4 t cell help and get t depdent antigen
