Quiz 4 Flashcards
(88 cards)
1
Q
What is the central cell in the primary immune response?
A
DC
2
Q
What is the central cell in the secondary immune response?
A
T/B cells
3
Q
What 3 things is special about the secondary immune response?
A
diversity
specificity
memory
4
Q
What are the 4 steps of the primary immune response?
A
- antigen—DC interactions
- DC—T cell interactions
- antigen—B cell interactions
- T cell—B cell interactions
5
Q
What are the 3 functions of DCs?
A
- pathogen recognition via PRR
- phagocytosis using PRR
- antigen processing
6
Q
Which MHC presents intracellular pathogens?
A
MHC I
7
Q
Which MHC presents extracellular pathogens?
A
MHC II
8
Q
Where are MHC I peptides loaded?
A
ER
9
Q
Where are MHC II peptides loaded?
A
vesicles
10
Q
What MHC does CD8+ T cells recognize?
A
MHC I
11
Q
What MHC does C4+ T cells recognize?
A
MHC II
12
Q
What cells express MHC I?
A
all cells
13
Q
What cells express MHC II?
A
macrophages
DC
B cells
TEC
14
Q
What does the symmetry of MHC I look like?
A
asymmetrical
15
Q
What does the symmetry of MHC II look like?
A
symmetrical
16
Q
Does MHC I or II bind smaller peptides?
A
MHC I
17
Q
Where does mature DC go after interacting with pathogen?
A
SLT
18
Q
What does DC present antigens on?
A
MHC II
19
Q
What cell does DC present to?
A
T cells
20
Q
What co-stimulatory molecule do DCs upregualte when presenting to T cells?
A
B7
21
Q
Where is the location of antigen presentation & B/T cell interactions?
A
SLT
22
Q
How do T cells come across a DC presenting an antigen?
A
They flow through the blood and SLT and will stay in the SLT if it comes across the DC presenting it will stay and differentiate and proliferate
23
Q
What 3 ligand/receptor interactions happen when a T cell interacts with a DC?
A
- TCR—MHC
- CD4 or CD8 —-MHC
- CD28—B7
24
Q
What autocrine cytokine signaling induces T cell proliferation?
A
IL-2
25
What 3 things can T cell differentiate into?
cytotoxic T cells
T regs
T helper
26
What allows isotype switching and SHM in BCR?
RNA splicing of heavy chain
27
memory and naive B cells express membrane bound ______
IgG
28
Naive B cells specifically express membrane bound _____ and _____
IgM
IgD
29
Where does class switching occur on BCR?
Fc regions heavy chain
30
B cells present to T cells which is required for...
T cell dependent B cell activation
31
What are the 3 ligand/receptor interactions that occur when B and T cells interact?
1. TCR---MHC
2. CD4---MHC
3. CD40-L---CD40
32
T cells upregulate _______ that interact with CD-40 on B cells
CD40-L
33
What is it called when a T cell and B cell are interacting?
conjugate pair
34
Where do B cells undergo SHM and isotype switching in the body?
germinal centers
35
What do memory B cells express?
membrane bound BCR
36
Do memory B cell receptors undergo class switching and SHM?
a little but not much
37
Do plasma cells BCR under class switching and SHM?
yes
38
What type of B cells are inactivated during the secondary immune response and why?
naive B cells
they are very broad and we already have a specific antibody from primary exposure
39
What are the 3 isotypes involved in Type II HSR?
IgG1
IgG3
IgM
40
What does IgG1 and IgG3 do?
opsonize
activate NK cells
activate complement
41
What does IgM do?
activate complement
42
What are the 3 effector function of type II HSR?
apoptosis
lysis
phagocytosis
43
What is the definition of a type II HSR?
IgM/IgG recognizes innocuous cell surface molecules as foreign, leading to antibody-mediated cell death via 3 mechanisms
44
What are the 3 mechanisms that cause cell death in type II HSR?
1. Ab-mediated complement activation = MAC
2. ADCC via NK cells
3. Ab-mediated opsonization = phagocytosis
45
What Ig isotype is responsible for the Ab-mediated complement activation mechanism in type II HSR?
IgM
46
What part of IgM binds to pathogen surface for complement activation?
Fab
47
What part of IgM recognizes C1q in complement activation?
Fc region
48
What is activated that leads to MAC formation?
C5 convertase
49
What conformational change occurs to IgM for complement activation?
pentameric IgM curls "staples"
50
What are the steps of complement activation?
1. C1q binds to antigen bound IgM
2. IgM conformational change = activation of C1r and Crs
3. C3 convertase hydrolyzes C3
4. C5 convertase formed
5. C1s cleaves C4 & C2 & C4b binds C2 exposing C1s
6. C1s cleaves C2 = c4b2a
7. C3b (in C5 convertase) binds to C5 = C4b2a cleaving C5 into C5a and C5b
8. C5b starts MAC complex
51
What is the key molecule in complement that starts the MAC complex?
C5b
52
What Ig isotype is mainly used in ADCC?
IgG1
53
What region of Ab bind to pathogen's surface?
Fab
54
What receptor do NK cells express during ADCC that binds to Ab Fc region?
FcGRII
55
What 2 things do NK cells release in ADCC?
granzymes and perforin
56
What is the steps of Fas-L/Granzyme mechanism?
1. Fas-L activates caspace-8
2. granzyme B & caspace-8 cleaves Bid
3. Bid mediates the release of cytochrome c
4. granzyme-b is cleaved = activation caspace-3
5. apoptosis
57
How do Ab function as an opson?
coats pathogen surface to be phagocytosed
58
Phagocytes have ___ receptors so it can bind to Ab when its acting as a opsin
Fc receptors
59
What are 2 phagocytes?
macrophages
neutrophils
60
What digests pathogens in phagocytes?
lysosomes
61
What are 3 types of type II HSR?
1. mismatch blood transfusions
2. hemolytic disease in newborns
3. drug induced anemia
62
What happens during a mismatch blood transfusions?
IgM binds to blood antigens (b/c its wrong) causing RBC lysis
63
What happens during hemolytic disease in newborns?
IgG responds to D-allele of Rh antigen
64
What happens during drug induced anemia?
IgM binds to RBC = RBC lysis
65
What Ig isotype is used in mismatched blood transfusions and drug induced anemia?
IgM
66
What 2 Type II HSR have the same mechanism?
mismatched blood transfusions
drug induced anemia
67
What enzymes do RBC express?
glycosyltransferase
68
What expressed on RBC makes the persons blood type?
glycoproteins
69
What individuals wont have hemolytic type II reactions and why?
type O
they lack A&B antigens
70
What is the only small difference between blood types?
additions of one sugar
71
Most people express Ig___ Ab againsy blood carb antigens they don't express
IgM
72
Why do do people possess IgM against blood types they dont have?
common microbes express similar carb antigens that induce host B cell responses = Ab binding to A or B antigen that isn't thier own
73
What Ig isotype mediates complement mediated lysis of RBC?
IgM
74
What is dangerous about RBC lysis?
high levels of hemoglobin that breaks down into porphyrin which metabolizes to toxic billirubin
75
Why is the fetus being Rh+ (D-allele) not an issue before the child is born?
there are little Rh+ RBC that are passed from bay to mother so no immune response happens
76
When does having an Rh+ baby and Rh- mother become and issue and why?
at birth when blood mixes
Rh+ baby blood induces an IgM immune response in the Rh- mother to clear the Rh+ fetal blood
77
How does the mother's immune system create protection for re-exposure of Rh+?
the mother will generate anti-D memory B cells which generate IgG for next exposure
78
Why is a mother's secondary exposure of D+ easier to achieve with fewer D+ RBC than the first exposure?
she has memory B cells which have a lower threshold for activation
79
In the secondary exposure of D+ RBC it takes _____ D+ RBC to activate an immune response
fewer
80
Ig___ cannot pass between placental barrier
IgM
81
Ig___ can pass the placental barrier
IgG
82
In hemolytic disease in fetus, Ig___ is responsible for the primary response while Ig___ is for the secondary response
IgM
IgG
83
Why is it dangerous that IgG can cross the placental barrier?
IgG is responsible for the secondary response (MEMORY) and is able to cross the barrier
- very dangerous for 2nd pregnancy
84
What does it mean the fetal RBC are attacked?
mothers anti-D antibodies bind to fetal Rh+ RBC and fetus own NK cells lyse fetal RBC
85
Rhogam is given during _______ pregnancy to prevent mother's Ab for binding to fetal RBCs
first
86
Why is Rhogam given to mothers 24-28 weeks in pregnancy?
almost complete maturation of fetal immune system
87
How does Rhogam therapy work?
contains anti-RH (D antigen) Ab that bind to fetal Rh+ RBC and inactivate fetal Rh before they stimulate an immune response in mother
88
What 2 ways does Rhogam prevent primary immune response to Rh+ RBC?
1. inhibit B cell signaling via FCGRIIB
2. Anti-D Ab binds to fetal RBC and is phagocytosed
