exam 5 Flashcards
(174 cards)
1
Q
humoral or cell mediated: what is best for extracellular and which is best for intercellular defense
A
humoral : extracellular
Cell mediated: intracellular
2
Q
what is clonal deletion
A
deleting self reactive B and T cells
3
Q
what is the precursors for macrophages and some dendritic
A
monocyte
4
Q
what is langerhan cells and where are they located
A
dendritic cells in skin
5
Q
list granulcytes
A
NEBM …. nuetrophil, eosinophil, basophil, mast
6
Q
who is the first responder in cell mediate innate immunity, what do they do
A
PMN luekocytes (nuetrophil)
-they phagocytosis and degranulation and make neutrophil extracellular traps
7
Q
basophil granules have what?
where are they located
A
histamine and heparin, go through the blood
8
Q
mast cells granules have what?
where are they located
A
histamine and heparin, found in tissue
9
Q
the right upper quadrant lymph drains where
A
right lyphatic duct
10
Q
The thoracic duct drain lymph from what part of the body
A
everywhere except the upper right quadrant because it is drained by right lymphatic duct
11
Q
name the APC cells
A
dendritic and macrophages B cells
12
Q
specialized CT is composed of
A
parenchyma (functional part) and stroma (structural part)
13
Q
the parenchyma has a large amount of what cell
A
lymphocytes
14
Q
the stroma has what kind of tissue
A
reticular tissue type 3 except the thymus
15
Q
what shape of cell in HEV
A
simple cuboidal
16
Q
HEV important role
A
extractivation of lymphocytes from blood to tissue
17
Q
Difference between primary and seconday lymph organs
A
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
18
Q
parenchyma in bone marrow is what type of cell
stroma is what kind of tissue
A
parenchyma: hemopoietic cells
stroma: reticular
19
Q
thymus
stroma is what kind of tissue
A
not reticular but has tight junction
20
Q
what cells found in the cortex of thymus
A
thymocyte( immature T)
thymic epithelial
macrophage
21
Q
where is thymocytes selected for immunocompetence
A
in the cortex of the thymus
22
Q
___% of thymocytes pass selection to become ____ cells or _____ cells
A
__2_% of thymocytes pass selection to become ___helpe cells___ or __cytotoxic t cells__
23
Q
what is thymic hassalls corpuscles
A
shows where the medulla is in the thymus
24
Q
Nodules indicate
A
adaptive immune response to antigen - secondary lympoid only not primary
25
challenged or unchallenged lypmphoid nodules and what does it mean
unchallenged - inactive T B cells and APC
26
challenged or unchallenged lymphoid nodules and what does it mean
challenged
27
red and yellow structure
yellow is primary red is secondary
28
what structure indicates b lymphocyte activation and proliferation
secondary lympoid
29
where are plasma cells and b memory cells made
germinal center of the secondary nodule
30
what does the difuse lyphoid tissue and tonsils survery
epithelial barriers
31
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
32
what tissue
MALT
33
Stroma of a lymphnode is made of
reticular CT
33
what is this and what is ABC
A- subcapsular
B-trabecular
C-Medullary
34
35
what tissue is found in the sinuses of the lymph node sinuses
reticular fibers
36
-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
37
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
38
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
39
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.
40
what are the primary functions of spleen
filter blood of ag
remove aged RBC
41
name yellow and white arrows and tissue or organ is this
Spleen
yellow is nodules
white is CT capsule
42
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
43
does spleen filter lymph
no
44
red pulp and white pulp which one is basophillic
red pulp is acidophillic
white is basophillic
45
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
46
Splenic chords are used for
getting rid of RBC
47
what cell activated White pulp
APC
48
what cell sursounds central arteriole (what organ)
T cells spleen
49
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
50
B - tonsils have epithelium
51
what is an immunogen
an antigent that binds to a receptor and elicits an immune response
52
whats a hapten
small anitgen that binds to receptor with no immune response
53
whats a mitogen
binds to receptor and induce cell division (polyclonal activator)
54
haptens can turn into _______
immunogens when conjugated
55
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
56
Tollergen vs immunogen
second exposure of immunogen
tollergen reduced immune response
immunogen increases immune response
57
what Ag is polyclonal activator
mitogen
58
some exotoxins from bacteria acts like a ______ antigen
super antigen - type of mitogen
59
what is an antigenic determinant
epitope
60
what is multivalent antigen vs polyvalent epitope
-antigen that has alot of copies of a single epitope
-antigen has different epitopes
61
the more complex an epitope the _____ he immune response
higher
62
what type of antigen creates polyclonal response
polyvalent ag
63
what is Adjuvants
substance that enhances immune response
64
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
65
What are PAMPS
pathogen associated patterns binds to PRP or TLR
66
what are TLR
type of PRR, recognize PAMPS leucin rich
67
what receptors are your adaptive immune
BCR and TCR
68
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
69
BCR is specific for ______ ag
TCR is specific for _______ ag
single for both
70
TLR are what type of receptor
PRR
71
Compliment is part of the of ________ immunity
innate humoral immunity
72
what pathway:
antibody to epitopes
classical
73
what pathway:
MBL - Mannose
Lectin pathway
74
what pathway:
cleaved c3 c3b - pathogen surface
allternative
75
what is the convergence point of the three pathways of the compliment response
c3 convertase
76
C3b leads to
opsonization
77
c5b-9
membrane attack complex MAC
78
c3a leads to
inflammation, and chemotaxis (a - stands for anaphylatoxins)
79
C4b
opsonization
80
factor 1 degrades what, how does the cleaved products act
c3b and c4b, can still function as opsons but no amplication of enzyme cascade
81
what does c5 convertase do
turns c5 to c5a (chemotaxis, inflammation) and c5b (Membrane attack lysis)
82
what is Hereditary angio edema HAE
deficiency in CN INH (C1inhibitor).... increased concentration of c3a C5a and thus excessive selling
-tx with recombinant C1INH
83
what is the C1 inhbitor
C1INH
84
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
85
what does DAF do
inactivates c3 convertase
86
what does CD59 do
inhibits MAC
87
cells in acute and chronic inflammation
ACUTE: neutrophils
CHRONIC: macrophages lymphocytes
88
vaso dilation is key feature of
innate response
89
Name inflamation mediators (plasma derived)
-compliment (c5a c3a chemotaxis)
-coagulation factors
-kinins
90
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
91
What releases NO
what releases cytokines
NO: endothelial
Cytokines: Macrophages
92
what is a inflammasome
reguates cytokine release
-cleaves pro-forms into active cytokines which matures IL1 IL18
**** novel target for anitinflammatory therapy
93
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
94
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
95
what mediates exravastion
CAMS
-selectins
-integrins
96
explain process of extravation
1. 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
97
describe expression difference of integrins and selectins
selectins always expressed
integrins espression increased by inflammatory mediators
98
what is the hallmark of chronic inflammation
infiltration of tissues with mononuclear cells
-monocytes macrophages and lymphocytes
99
What is M2 cells
macrophages that clean up coes form monocyte
100
what is granuloma
happens in chronic infection
- macrophage turns to epithliod cell
-surrounded by T and Fibroblasts
-has necrotic center
-can cause re-infection
101
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
102
How does NSAIDS work
block prostogladins and thromboxane that came from arachidonic acid (which is a cell derived mediator)
-so limit vasculatory permeability
103
how does corticosteroids
basically decreased everything so immuno supressed
104
How does Anti-TNF nuetralizing agent work
binds to TNF-a
blocks it from going to receptor at site of infection
105
Anti CAM antibodies
blocks integrin ICAM interaction preventing extravation
106
When does CT/scar occur
-ecm damaged
-stem cells lost
-tissue lacks proliferative regen capabilities
HEART
107
what two supplements are needed for scarring and why
VIT C
COPPER
- both for cross linking of collagen formation
108
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)
109
what are stable cells, list examples
MIN PROLIFERATIVE
-liver
-kidney
-pancreas
110
what are permanent cells, list examples
NO PROLIFERATION
-nuerons
-cardiac
-skelatal
-lens
111
Transforming GF (TGF -beta)
collagen formation via stimulation of fibroblast
112
Vascular Endothelial GF (VEGF)
-vascular permeability
-important for angiogen
-key in granulation
113
Platelet Derived GF (PDGF)
-angiogenesis
114
Fibroblast BF (FGF)
angiogen
wound contraction
115
what growth factor and cells is important for wound contraction
FGF and myofibroblasts
116
What growth factors for angiogen
VEGF
FGF
PDGF
117
what is the hallmark of tissue healing
granulation
118
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
119
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
120
what are MMPs
matric metalloproteinases
- breakdown ECM
121
what is myofibroblast
it causes wound contraction
122
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
123
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
124
Gluco-corticosteroids role in wound healing
hormone delays healing... causes weak scar
- decrease inflammatory response....
inhibit TGF-Beta which inhibits collagen synthesis
weak scar
125
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
126
Fibrosis occurs where
parenchymal organ
127
Keloids is made of what
collagen 3
128
contraction of large surface wounds is due to what cell
myofibroblasts
129
what do you need to know about this image
130
what do you need to know about this image
131
what enzymes responsible for would repair
MMPs
132
what cell is pattern recognition receptors found
they are receptors on phagocytes
133
Name two types of PRR receptos and what they do
-PAMPS receptors
(pathogen associated molecular pathogens...)
-Opsonin receptors
134
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)
135
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
136
APC activate what cell
T helper and cytotoxic t cells via t cell recepetor
137
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
138
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
139
Each person has how many haplotypes?
what is a haplotype
2 haplotypes
HLA haplotype is a set of hc alleles
140
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
141
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
142
What is TAP deficiency
They have a reduced MHC 1 meaning reduction of cd8 t cll muturation and function
143
what cell can cross present and what receptors do they present
Dendritic for tumor cells MHC 1 and MHC 12
144
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)
145
Ch Cl Vh Vl what are they
Ch Cl they are the constant region
Vh VL are the variable region
146
what region is responsible for antigen binding
both heavy and light chain variable region
147
what region is responsible for isotype of antibody
contant region of the heavy chain only
148
signaling portion of the bcr
Igalpha Igbeter
149
What is antiserum
serm that have alot of antibodies
150
what type of anitbodies activate classical pathway of compliment
IgM IgG
151
what region of antibody is needed for opsonization
Fc
152
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
153
what two antibodies cross link degranulation happens
IgE
154
what two antibodies have J chain
IgM pentamer and IgA dymer
155
IgA
in Tears and breast milk and saliva external secretion
156
IgD
activates Basophils and mast cells, membrane bound
157
IgE
against worms and allergic reaction
158
IgG
secreated by plasma cells and can cross placenta
159
IgM
may attach to surface of B cell or secreted into blood. EARLY STAGE immunity
160
what cell is the first antibody secreted during primary response what percent is in serum
5-10% IgM
161
Ab secreted suring memory response what percent is in serum
IgG 8-%
162
which illicites a stronger immune response linear or folded
folded
163
what INF stimulates NK cells
is it innate or adaptive
beta, innate
164
what inf stimulates nuetrophyl
gama
165
what cell is hallmark for chronic inflammation
macrophages
166
what do INF1 alpha and beta do
antiviral
rnase
viral replication halted
NK activity
increase MHC1 expression
167
name granules of nk cells
perforin - makes pore
granzyme - induce apoptosis
168
do cytokines regulate innate or adaptive
both
169
what is NF-kb
inflammation transcription factor
170
what is IRF-3
transcription factor that is antiviral, makes cell release INF alpha aand beta
171
what is IL12
macrophage secrete it cause they cant digest microorganism. this activates NK cells
172
what is INF y (gama)
secreted by NK cells to microbicidal activity to macrophages
173
