exam 5 Flashcards
humoral or cell mediated: what is best for extracellular and which is best for intercellular defense
humoral : extracellular
Cell mediated: intracellular
what is clonal deletion
deleting self reactive B and T cells
what is the precursors for macrophages and some dendritic
monocyte
what is langerhan cells and where are they located
dendritic cells in skin
list granulcytes
NEBM …. nuetrophil, eosinophil, basophil, mast
who is the first responder in cell mediate innate immunity, what do they do
PMN luekocytes (nuetrophil)
-they phagocytosis and degranulation and make neutrophil extracellular traps
basophil granules have what?
where are they located
histamine and heparin, go through the blood
mast cells granules have what?
where are they located
histamine and heparin, found in tissue
the right upper quadrant lymph drains where
right lyphatic duct
The thoracic duct drain lymph from what part of the body
everywhere except the upper right quadrant because it is drained by right lymphatic duct
name the APC cells
dendritic and macrophages B cells
specialized CT is composed of
parenchyma (functional part) and stroma (structural part)
the parenchyma has a large amount of what cell
lymphocytes
the stroma has what kind of tissue
reticular tissue type 3 except the thymus
what shape of cell in HEV
simple cuboidal
HEV important role
extractivation of lymphocytes from blood to tissue
Difference between primary and seconday lymph organs
Primary
- thymus and bone marrow make B & T cells
-B cells stay in bone marrow
-T cells mature in thymus
Secondary
- where immune response occurs
-spleen tonsils lymph nodes
parenchyma in bone marrow is what type of cell
stroma is what kind of tissue
parenchyma: hemopoietic cells
stroma: reticular
thymus
stroma is what kind of tissue
not reticular but has tight junction
what cells found in the cortex of thymus
thymocyte( immature T)
thymic epithelial
macrophage
where is thymocytes selected for immunocompetence
in the cortex of the thymus
___% of thymocytes pass selection to become ____ cells or _____ cells
__2_% of thymocytes pass selection to become ___helpe cells___ or __cytotoxic t cells__
what is thymic hassalls corpuscles
shows where the medulla is in the thymus
Nodules indicate
adaptive immune response to antigen - secondary lympoid only not primary
challenged or unchallenged lypmphoid nodules and what does it mean
unchallenged - inactive T B cells and APC
challenged or unchallenged lymphoid nodules and what does it mean
challenged
red and yellow structure
yellow is primary red is secondary
what structure indicates b lymphocyte activation and proliferation
secondary lympoid
where are plasma cells and b memory cells made
germinal center of the secondary nodule
what does the difuse lyphoid tissue and tonsils survery
epithelial barriers
Tonsils are made of what tissue? describe structure and components
MALT (mucosa associated lymphoid)
-No cortex or capscle or medulla
-randomy packed B and T lymphocytes
-crypts
-nodules
- epithelium
what tissue
MALT
Stroma of a lymphnode is made of
reticular CT
what is this and what is ABC
A- subcapsular
B-trabecular
C-Medullary
what tissue is found in the sinuses of the lymph node sinuses
reticular fibers
-The outer cortex of the lymph node is what kind of teritorritory
-the deep cortex is what kind of teritorritory
Outer- nodule houses B cell
deep cortex is T cell and HEV extravation
name the blue red and dotted yellow, green
where are T , B and HEV located
Yellow dotted: nodule
red: is outer cortex
blue is deep cortex
green: medullary cord
T is in the deep cortex
B is in nodule
HEV is in deep cortex
explain the route of a lymphocyte in lymphnode
B T come in through artery, enter lymph node through HEV, T stay in cortex, B cells go to outer cortex and form noduled. APC activate T helper cells. T cells activate B cells to make them into plasma cells (germinal center) . Plasma cell goes to medulallary since and exit efferent vessels
what forms the medullary cord and what does the medullary cord do
it is made of parenchyma cells
macrophages, lymphocytes and plasma cells stey here.
what are the primary functions of spleen
filter blood of ag
remove aged RBC
name yellow and white arrows and tissue or organ is this
Spleen
yellow is nodules
white is CT capsule
name the red and white dots
what tissue or organ is this
Red dot = red pulp : blood filled caillaries and splenic cords
White dot = white pulp: lymphoid nodules
does spleen filter lymph
no
red pulp and white pulp which one is basophillic
red pulp is acidophillic
white is basophillic
describe how the filtration of antigen and old rbc
In spleen
-Trabecular art
-Central art
-penicillar arteriols
-dump blood into splenic cords of the red pulp
-goes to venous circulation via sinusoidal capillaries
Splenic chords are used for
getting rid of RBC
what cell activated White pulp
APC
what cell sursounds central arteriole (what organ)
T cells spleen
what is this showing. explain the steps
white pulp response to ag.
1. APC in the red chored activate T helper in the PALS
2. T helper activate B cceels
3. primary nodules expand &push pals
4. B cells proliferate secondary nodule
5. plasma and memory B cells into sinusoid
B - tonsils have epithelium
what is an immunogen
an antigent that binds to a receptor and elicits an immune response
whats a hapten
small anitgen that binds to receptor with no immune response
whats a mitogen
binds to receptor and induce cell division (polyclonal activator)
haptens can turn into _______
immunogens when conjugated
explain clincal application hemolytic anemia
antibiotic are haptens but they absorb and bind to proteins on RBC surface making an immunogen that make RBC lysis = Jaundice
Tollergen vs immunogen
second exposure of immunogen
tollergen reduced immune response
immunogen increases immune response
what Ag is polyclonal activator
mitogen
some exotoxins from bacteria acts like a ______ antigen
super antigen - type of mitogen
what is an antigenic determinant
epitope
what is multivalent antigen vs polyvalent epitope
-antigen that has alot of copies of a single epitope
-antigen has different epitopes
the more complex an epitope the _____ he immune response
higher
what type of antigen creates polyclonal response
polyvalent ag
what is Adjuvants
substance that enhances immune response
what are PRR where are they located? Innate or adaptive
receptor from innate systme, that recognizes (PAMPS - pathogen associated pattern) NON specific
-located in and out of cell
What are PAMPS
pathogen associated patterns binds to PRP or TLR
what are TLR
type of PRR, recognize PAMPS leucin rich
what receptors are your adaptive immune
BCR and TCR
what is the difference between B cell receptors and T cell receptors
B cell-
-membrane bound immunoglobulin on the surface
-receptors can be secreted as antibodies
-bind many types of shapes ag
T Cells
-tcr bind only linear peptride ag displayed on MHC
BCR is specific for ______ ag
TCR is specific for _______ ag
single for both
TLR are what type of receptor
PRR
Compliment is part of the of ________ immunity
innate humoral immunity
what pathway:
antibody to epitopes
classical
what pathway:
MBL - Mannose
Lectin pathway
what pathway:
cleaved c3 c3b - pathogen surface
allternative
what is the convergence point of the three pathways of the compliment response
c3 convertase
C3b leads to
opsonization
c5b-9
membrane attack complex MAC
c3a leads to
inflammation, and chemotaxis (a - stands for anaphylatoxins)
C4b
opsonization
factor 1 degrades what, how does the cleaved products act
c3b and c4b, can still function as opsons but no amplication of enzyme cascade
what does c5 convertase do
turns c5 to c5a (chemotaxis, inflammation) and c5b (Membrane attack lysis)
what is Hereditary angio edema HAE
deficiency in CN INH (C1inhibitor)…. increased concentration of c3a C5a and thus excessive selling
-tx with recombinant C1INH
what is the C1 inhbitor
C1INH
what is paroxymal noctural hemoglobinuria
deficiency in DAF and CD59 on RBC . CD59 inhibits MAC
DAF inactivates c3 convertase
leads to c3 convertase always on and MAC formation
causing
meolytic enemia
what does DAF do
inactivates c3 convertase
what does CD59 do
inhibits MAC
cells in acute and chronic inflammation
ACUTE: neutrophils
CHRONIC: macrophages lymphocytes
vaso dilation is key feature of
innate response
Name inflamation mediators (plasma derived)
-compliment (c5a c3a chemotaxis)
-coagulation factors
-kinins
what is arachidoonic acid and where is derived and made
-cell derived inflammation mediator
-from wbc and injured cells
-vasodilator that fx with fever and pain
What releases NO
what releases cytokines
NO: endothelial
Cytokines: Macrophages
what is a inflammasome
reguates cytokine release
-cleaves pro-forms into active cytokines which matures IL1 IL18
** novel target for anitinflammatory therapy
what is acute phase protein
cytokines make liver realease these proteins causing a 25% increase in inflamation RBC to sediment fast and increased ESR and CRP
What is CRP
most sensitie acute phase protein
useful marker to show how bad inflammation including course
-activates complement
-stimulates release of cytokines from phagocytes
what mediates exravastion
CAMS
-selectins
-integrins
explain process of extravation
- rolling adhesion
wbs attatched to endothelial cells via selectins
2.stable adhesion (stop them at site of infection)
wbc attatched to endothelial cells via integrins
describe expression difference of integrins and selectins
selectins always expressed
integrins espression increased by inflammatory mediators
what is the hallmark of chronic inflammation
infiltration of tissues with mononuclear cells
-monocytes macrophages and lymphocytes
What is M2 cells
macrophages that clean up coes form monocyte
what is granuloma
happens in chronic infection
- macrophage turns to epithliod cell
-surrounded by T and Fibroblasts
-has necrotic center
-can cause re-infection
Valley fever clinical relavence
granuloma
happens in chronic infection
- macrophage turns to epithliod cell
-surrounded by T and Fibroblasts
-has necrotic center
-can cause re-infection
How does NSAIDS work
block prostogladins and thromboxane that came from arachidonic acid (which is a cell derived mediator)
-so limit vasculatory permeability
how does corticosteroids
basically decreased everything so immuno supressed
How does Anti-TNF nuetralizing agent work
binds to TNF-a
blocks it from going to receptor at site of infection
Anti CAM antibodies
blocks integrin ICAM interaction preventing extravation
When does CT/scar occur
-ecm damaged
-stem cells lost
-tissue lacks proliferative regen capabilities
HEART
what two supplements are needed for scarring and why
VIT C
COPPER
- both for cross linking of collagen formation
what are Libile cells, list examples
HIGH PROLIFERATIVE CELLS
-epithelium in skin (stem cells @ basal layer) GIT (@crypts)
-Bonemarrow - (hematopoetic stem cells)
-corneal epithelium - (@limbus)
what are stable cells, list examples
MIN PROLIFERATIVE
-liver
-kidney
-pancreas
what are permanent cells, list examples
NO PROLIFERATION
-nuerons
-cardiac
-skelatal
-lens
Transforming GF (TGF -beta)
collagen formation via stimulation of fibroblast
Vascular Endothelial GF (VEGF)
-vascular permeability
-important for angiogen
-key in granulation
Platelet Derived GF (PDGF)
-angiogenesis
Fibroblast BF (FGF)
angiogen
wound contraction
what growth factor and cells is important for wound contraction
FGF and myofibroblasts
What growth factors for angiogen
VEGF
FGF
PDGF
what is the hallmark of tissue healing
granulation
what cells found in granulation?
when does granulation start and peaks?
macrophage inflammatory cells and fibroblasts
starts at day 3
Peak at 5 -7 days
when does ecm deposition occur?
what is ECM?
When does it start and end?
collagen synthesis TGF beta, PDGF, FGF
start 3-5 days
ddense collagen pale is 1 month
what are MMPs
matric metalloproteinases
- breakdown ECM
what is myofibroblast
it causes wound contraction
explain various times of wound strengthing
-end of 1 week : 10 tensile strength
-2 mo increase of ensil due to type 3 collagen increase
-synthesis stops for stucture modification of collagen fibers type 1 collagen
-end of 3 months: PLATUE maximum tensile strength 70-80% normal
Difference of first and second intention healing
-first is bringing edges together like suture very little scar
ONLY epithelial layer
-second is not being able to close more inflammation large scar
Gluco-corticosteroids role in wound healing
hormone delays healing… causes weak scar
- decrease inflammatory response….
inhibit TGF-Beta which inhibits collagen synthesis
weak scar
Compare contrast keloids and hyper trophic scar
-both dues to excess formation of collagen
-Keloids
goes out side boundary of wound
does ot regress
recur after surgical resection
genetic predisposition
-Hypertrophic scar
stays in boundries in wound
regresses
Fibrosis occurs where
parenchymal organ
Keloids is made of what
collagen 3
contraction of large surface wounds is due to what cell
myofibroblasts
what do you need to know about this image
what do you need to know about this image
what enzymes responsible for would repair
MMPs
what cell is pattern recognition receptors found
they are receptors on phagocytes
Name two types of PRR receptos and what they do
-PAMPS receptors
(pathogen associated molecular pathogens…)
-Opsonin receptors
difference oxygen dependent and oxygen independent digestion
done by phagocytes
OXYGEN INDEPENDENT
-proteolytic enzyme
OXYGEN DEPENDENT
-uses reactive oxygen intermediates ROIS and Reactive nitrogen species (RNS)
explain clinical relavence. whats left and right?
Granulomatous disease X linked —–defect in production of NADPH
-meaning inefficient killing
-granuloma formation
-right enzyme activity
-left no enzyme
APC activate what cell
T helper and cytotoxic t cells via t cell recepetor
MHC1
stucture:
type of antigen - exo or exracellular
or endogenous/ intracellular:
Cells that express this:
T cell subset that will bind:
HLA gene:
Gene expression:
MHC1
stucture: 1 variable alpha and one non variable B2 microglbulin
**type of antigen - exo or exracellular
or endogenous/ intracellular: ** endogenous - cytoplasmic peptides
intracellular
Cells that express this: all nucleated cells
T cell subset that will bind: Tc cd-8
HLA gene: HLA-A HLA-B HLA-C
Gene expression: poly morphic (different allels for each gene) polygenic three genes for each class
MHC2
stucture:
type of antigen - exo or exracellular
or endogenous/ intracellular:
Cells that express this:
T cell subset that will bind:
HLA gene:
Gene expression:
MHC2
stucture: variable alpha and B2 microglbulin
**type of antigen - exo or exracellular
or endogenous/ intracellular: ** exogenous
extracellular
Cells that express this: APC
T cell subset that will bind: Th CD-4
HLA gene: HLA-DP HLA-DQ HLA-DR
Gene expression:
poly morphic (different allels for each gene) polygenic three genes for each class
Each person has how many haplotypes?
what is a haplotype
2 haplotypes
HLA haplotype is a set of hc alleles
Cytosolic pathway
what MHC and explain process
MHC 1 for Tc cells
* breakdown endoenous protein in cytosol via proteosomes
* TAP transporter to RER membrane
* synthesize mhc 1 and processing protein in REER
* peptide goes in cleft
* MHC and peptide go to cell membrane for cytotoxic cells to recognize on CD8 receptor
Endocytic pathway
what MHC and explain process
MHC 2 for Th
* lysosomal degradation of endocytosed antigen
* sythesis of MHC 2 and invariant chain Ii in RER
* degrade Ii from binding cleft
* HLA DM helps load exogenous peptde into MHC 2 cleft
* go to cell membrain for Th cells with cd4
What is TAP deficiency
They have a reduced MHC 1 meaning reduction of cd8 t cll muturation and function
what cell can cross present and what receptors do they present
Dendritic for tumor cells MHC 1 and MHC 12
what is recognition phase and what is effector phase
2 phases of antibodies - humoral immunity
recognition: membrane bound antibodies B cell receptors
effector: secreted by effector B cells (plasma cells)
Ch Cl Vh Vl what are they
Ch Cl they are the constant region
Vh VL are the variable region
what region is responsible for antigen binding
both heavy and light chain variable region
what region is responsible for isotype of antibody
contant region of the heavy chain only
signaling portion of the bcr
Igalpha Igbeter
What is antiserum
serm that have alot of antibodies
what type of anitbodies activate classical pathway of compliment
IgM IgG
what region of antibody is needed for opsonization
Fc
what are the two andibodies used for antibody dependent cell mediate cytotoxicity
- IgG sits on the surface of the cell and NK kill it
- IgE on helminth and eosinophil kill it
what two antibodies cross link degranulation happens
IgE
what two antibodies have J chain
IgM pentamer and IgA dymer
IgA
in Tears and breast milk and saliva external secretion
IgD
activates Basophils and mast cells, membrane bound
IgE
against worms and allergic reaction
IgG
secreated by plasma cells and can cross placenta
IgM
may attach to surface of B cell or secreted into blood. EARLY STAGE immunity
what cell is the first antibody secreted during primary response what percent is in serum
5-10% IgM
Ab secreted suring memory response what percent is in serum
IgG 8-%
which illicites a stronger immune response linear or folded
folded
what INF stimulates NK cells
is it innate or adaptive
beta, innate
what inf stimulates nuetrophyl
gama
what cell is hallmark for chronic inflammation
macrophages
what do INF1 alpha and beta do
antiviral
rnase
viral replication halted
NK activity
increase MHC1 expression
name granules of nk cells
perforin - makes pore
granzyme - induce apoptosis
do cytokines regulate innate or adaptive
both
what is NF-kb
inflammation transcription factor
what is IRF-3
transcription factor that is antiviral, makes cell release INF alpha aand beta
what is IL12
macrophage secrete it cause they cant digest microorganism. this activates NK cells
what is INF y (gama)
secreted by NK cells to microbicidal activity to macrophages
