Immunology Test Questions with
Verified Solutions
* What happens to a single-positive CD4 thymocyte whose TCR does not bind to a
peptide presented with MHC by a thymic dendritic cell (DC)?
A) thymocyte does not bind to cTEC
B) thymocyte binds with low affinity to cTEC
C) thymocyte does not bind to mTEC
D) thymocyte binds with high affinity to mTEC
What happens to a double-positive thymocyte whose TCR binds with low affinity to a
peptide presented with MHC I by a cortical thymic epithelial cell (cTEC)?
What happens to a double-positive thymocyte whose TCR binds with high affinity to a
peptide presented with MHC I by a cortical thymic epithelial cell (cTEC)? - correct
Answer-it becomes a mature naive CD4 T lymphocyte
A) Death by neglect (apoptosis)
B) positive selection of MHC-restricted thymocyte
C) positive selection of self-tolerant thymocyte
D) negative selection of auto-reactive thymocyte (apoptosis)
*We want weak binding to either MHC 1 or MHC 2 because strong binding indicates
that the T cell receptor binds to self MHC like its an antigen (It's recognizing self as an
antigen)
-Strong bind= negative selection = cell death
Part of self tolerance
it becomes an immature single-positive CD8 thymocyte
it undergoes apoptosis
*A Rh-negative mother can be given injections of an antibody therapy called
_____________ during pregnancy to prevent an anti-D response against her Rh-
positive fetus and resulting hemolytic disease of the newborn (HDN). - correct Answer-
RhoGAM
*Rh factor: D antigen (third antigen)
If you have it you are positive, if you don't have it you are negative
Rh positive is dominant
If you are negative, you would respond against blood that has it
,Not born with antibodies, have to be exposed first (first transfusion isn't a big deal)
More important during pregnancy: Rh negative mother who has Rh positive fetus
During first pregnancy he's not attacked
Mother devops immune response on second pregnancy that develops from memory
response reactivated from first pregnancy, she will produce antibodies against Rh
factors (can cross the placenta and enter fetal blood supply, and start attacking fetus
blood cells: can create hemolytic disease of newborn- develops into anemia (lack of
oxygen transported) - more severe with more pregnancies)
RhoGAM given: Antibody that blocks mothers antibodies
*Antigen Presentation - correct Answer-APC and cell that antigen is going to be
presented to (ALWAYS a T cell)
APC has MHC with Ag
How does T cell recognize presented antigen? It uses TCR (T cell receptor), which has
domains that recognize the antigen and self MHC presenting it
Co-receptor molecule goes from T cell, attaches to MHC
4 molecules: T-cell has co-receptor (recognizes class of MHC) and TCR
This results in intracellular signal via CD3 complex, and then T cell is stimulated, which
causes it to change in some way
When immature T cells arrive in thymus, they start showing T cell receptors and BOTH
CD4 and CD8 co-receptors (double positive thymocyte)
Here, it encounters APC (called a CTEC) presenting self antigens using MHC
At this stage, we are testing to see if TCR recognizes our MHC because in the future we
need it to work with our MHC
-CTEC: Does it recognize Self MHC? strong binding = recognize the self antigen or
recognizes the self MHC too strongly
-Weak binding = only recognizes self MHC, which is what we want (positive selection)
This whole process is called MHC restriction
Next stage: Selection
Same TCR, lets say its MHC 1, so we would have single positive CD8 thymocyte
Test receptor for binding to self antigens (moves to thymus medulla, where its exposed
to MTECs)
-If it recognizes antigen that is presented, you get apoptosis, because you don't want it
to attack your own tissues (attacking self)
-Negative selection = binding = apoptosis (remove thymocytes that recognize self
antigens)
-Positive selection: Surviving thymocytes become mature naive t-lymphocytes, that
travel to secondary lymphoid tissues
Problem with this system: mtecs present thymic antigens that they normally present, but
your self is made up of more than just thymus cells. There are also DCs that exist in the
thymus that are APCs, so now we can present antigens from
,*Autocrine signaling - correct Answer-When a cell produces cytokine, but cytokine binds
to its same receptor (self-stimulation)It starts producing more of that cytokine, and more,
and more, it's a cycle (Positive feedback loop)
*Cat Allergies
Cat allergy is an IgE-mediated response against the Fel d 1 antigen produced by cats.
What type of hypersensitivity is this?
The cat vaccine created by Thoms, et al. 2019 induced production of <CHOOSE
ANSWER> antibodies that neutralized the Fel d 1 antigen and reduced its presence in
cat secretions.
*Which Fc receptor on mast cells and basophils is responsible for binding allergen-
specific IgE? - correct Answer-Cat allergy is an IgE-mediated response against the Fel
d 1 antigen produced by cats. What type of hypersensitivity is this? Type 1
hypersensitivity
Characterized by TH2 response
The cat vaccine created by Thoms, et al. 2019 induced production of <CHOOSE
ANSWER> antibodies that neutralized the Fel d 1 antigen and reduced its presence in
cat secretions. IgG
*Which Fc receptor on mast cells and basophils is responsible for binding allergen-
specific IgE? Fc-Epsilon-R1
•Feld 1 is the major allergen
•Anti-Feld 1 IgE is found in blood of 80-95% of allergic patients
Don't react until second exposure, when degranulation is triggered, releasing histamine,
and causing inflammatory response
Research article: giving cats shots of allergen, hopefully limiting production of Fel d 1
before cat secretes it
The major problem that scientists had to overcome when vaccinating cats with Fel d 1
antigen was that Fel d 1 is a self antigen for cats, meaning that cats will not naturally
produce antibodies against it. So, in order to overcome self-tolerance and get the cats
to produce an antibody response, virus-like particles (VLPs) were used that act as a
carrier for PAMPs and antigens. Specifically, Fel d 1 was coated in the epitope of
tetanus toxin poke the cats immune system to overcome self tolerance and force IgG
antibody response (good neutralizer)
Successful in reducing amount of Fel d 1 secretions. This was shown because the
percent of basophil activation went down.
If Fel D 1 was in secretions it should have activated basophils, and the reduction in
activated basophils demonstrated a reduction in Fel D 1. This proves that the vaccine
was successful in stimulating an immune response.
, *Combinatorial Diversity - correct Answer-created by somatic recombination of
randomly-selected gene segments
TCR alpha and BCR Light (very similar) - No D region
VJ C
Alpha: 70 V segments, 61 J segments = 4270 possible combinations
To make the TCR, one random alpha + one random beta chain (similar to BCR heavy
chain with VDJC) to make antigen binding site (1352X 4270 = 5.8 X 10^6 possible
combination) (still just starting with two genes, alpha and beta) -But this won't cover
enough (there are more than 6 million antigens, not even thinking about how many
different epitopes on each antigen)
*Diapedesis - correct Answer-As neutrophils go by they form weak connections
(temporarily binds and breaks free), but this slows the neutrophils down (keeps hitting
things and slowing down), starts tumbling - temporary attraction = Rolling adhesion -
then when neutrophil has slowed down more, an interaction that is much tighter occurs
and stops
Neutrophil starts to flatten out so it can squeeze through gaps into tissue space
(extravasation) - getting from inside the blood vessel to outside - DIAPEDESIS is the
way in which this happens/ Process of changing shapeChemokines: chemicals that are
at highest concentration near source of infection- kind of like trail of breadcrumbs-
cause intracellular changes that cause cell shape changes-Pus = dead neutrophils +
exudate
*For activation of T cells and formation of long-term memory, T cells require three
signals during antigen presentation. The three signals include - (signal 1) antigen
binding to the T cell receptor, (signal 2) <CHOOSE ANSWER> and (signal 3) cytokine
signaling from the APC and other innate cells. - correct Answer-co-stimulation by CD28
*B7 CD28: Used for Naive (found on APC)
CD28 is found on Th1 or Th2-cells
B7-CD28 interaction occurs when APC with antigen, presents to a T-cell to activate that
T-cell.
CD40L-CD40 interaction occurs when a helper T cell (CD-40L) activates a B-cell to
initiate class switching and antibody production.
*For variolation, the process of introducing a microbe or its antigens into a patient is
called: - correct Answer-Inoculation
The most common method was to use a needle to retrieve material from pustules from
a patient with variola minor and then stick the recipient in the arm with that needle.
*Granulocytes - correct Answer-Includes neutrophils, eosinophils, basophils, mast
cellsInnate immune cells that produce and respond to inflammatory signals.
-Second line of defense
Verified Solutions
* What happens to a single-positive CD4 thymocyte whose TCR does not bind to a
peptide presented with MHC by a thymic dendritic cell (DC)?
A) thymocyte does not bind to cTEC
B) thymocyte binds with low affinity to cTEC
C) thymocyte does not bind to mTEC
D) thymocyte binds with high affinity to mTEC
What happens to a double-positive thymocyte whose TCR binds with low affinity to a
peptide presented with MHC I by a cortical thymic epithelial cell (cTEC)?
What happens to a double-positive thymocyte whose TCR binds with high affinity to a
peptide presented with MHC I by a cortical thymic epithelial cell (cTEC)? - correct
Answer-it becomes a mature naive CD4 T lymphocyte
A) Death by neglect (apoptosis)
B) positive selection of MHC-restricted thymocyte
C) positive selection of self-tolerant thymocyte
D) negative selection of auto-reactive thymocyte (apoptosis)
*We want weak binding to either MHC 1 or MHC 2 because strong binding indicates
that the T cell receptor binds to self MHC like its an antigen (It's recognizing self as an
antigen)
-Strong bind= negative selection = cell death
Part of self tolerance
it becomes an immature single-positive CD8 thymocyte
it undergoes apoptosis
*A Rh-negative mother can be given injections of an antibody therapy called
_____________ during pregnancy to prevent an anti-D response against her Rh-
positive fetus and resulting hemolytic disease of the newborn (HDN). - correct Answer-
RhoGAM
*Rh factor: D antigen (third antigen)
If you have it you are positive, if you don't have it you are negative
Rh positive is dominant
If you are negative, you would respond against blood that has it
,Not born with antibodies, have to be exposed first (first transfusion isn't a big deal)
More important during pregnancy: Rh negative mother who has Rh positive fetus
During first pregnancy he's not attacked
Mother devops immune response on second pregnancy that develops from memory
response reactivated from first pregnancy, she will produce antibodies against Rh
factors (can cross the placenta and enter fetal blood supply, and start attacking fetus
blood cells: can create hemolytic disease of newborn- develops into anemia (lack of
oxygen transported) - more severe with more pregnancies)
RhoGAM given: Antibody that blocks mothers antibodies
*Antigen Presentation - correct Answer-APC and cell that antigen is going to be
presented to (ALWAYS a T cell)
APC has MHC with Ag
How does T cell recognize presented antigen? It uses TCR (T cell receptor), which has
domains that recognize the antigen and self MHC presenting it
Co-receptor molecule goes from T cell, attaches to MHC
4 molecules: T-cell has co-receptor (recognizes class of MHC) and TCR
This results in intracellular signal via CD3 complex, and then T cell is stimulated, which
causes it to change in some way
When immature T cells arrive in thymus, they start showing T cell receptors and BOTH
CD4 and CD8 co-receptors (double positive thymocyte)
Here, it encounters APC (called a CTEC) presenting self antigens using MHC
At this stage, we are testing to see if TCR recognizes our MHC because in the future we
need it to work with our MHC
-CTEC: Does it recognize Self MHC? strong binding = recognize the self antigen or
recognizes the self MHC too strongly
-Weak binding = only recognizes self MHC, which is what we want (positive selection)
This whole process is called MHC restriction
Next stage: Selection
Same TCR, lets say its MHC 1, so we would have single positive CD8 thymocyte
Test receptor for binding to self antigens (moves to thymus medulla, where its exposed
to MTECs)
-If it recognizes antigen that is presented, you get apoptosis, because you don't want it
to attack your own tissues (attacking self)
-Negative selection = binding = apoptosis (remove thymocytes that recognize self
antigens)
-Positive selection: Surviving thymocytes become mature naive t-lymphocytes, that
travel to secondary lymphoid tissues
Problem with this system: mtecs present thymic antigens that they normally present, but
your self is made up of more than just thymus cells. There are also DCs that exist in the
thymus that are APCs, so now we can present antigens from
,*Autocrine signaling - correct Answer-When a cell produces cytokine, but cytokine binds
to its same receptor (self-stimulation)It starts producing more of that cytokine, and more,
and more, it's a cycle (Positive feedback loop)
*Cat Allergies
Cat allergy is an IgE-mediated response against the Fel d 1 antigen produced by cats.
What type of hypersensitivity is this?
The cat vaccine created by Thoms, et al. 2019 induced production of <CHOOSE
ANSWER> antibodies that neutralized the Fel d 1 antigen and reduced its presence in
cat secretions.
*Which Fc receptor on mast cells and basophils is responsible for binding allergen-
specific IgE? - correct Answer-Cat allergy is an IgE-mediated response against the Fel
d 1 antigen produced by cats. What type of hypersensitivity is this? Type 1
hypersensitivity
Characterized by TH2 response
The cat vaccine created by Thoms, et al. 2019 induced production of <CHOOSE
ANSWER> antibodies that neutralized the Fel d 1 antigen and reduced its presence in
cat secretions. IgG
*Which Fc receptor on mast cells and basophils is responsible for binding allergen-
specific IgE? Fc-Epsilon-R1
•Feld 1 is the major allergen
•Anti-Feld 1 IgE is found in blood of 80-95% of allergic patients
Don't react until second exposure, when degranulation is triggered, releasing histamine,
and causing inflammatory response
Research article: giving cats shots of allergen, hopefully limiting production of Fel d 1
before cat secretes it
The major problem that scientists had to overcome when vaccinating cats with Fel d 1
antigen was that Fel d 1 is a self antigen for cats, meaning that cats will not naturally
produce antibodies against it. So, in order to overcome self-tolerance and get the cats
to produce an antibody response, virus-like particles (VLPs) were used that act as a
carrier for PAMPs and antigens. Specifically, Fel d 1 was coated in the epitope of
tetanus toxin poke the cats immune system to overcome self tolerance and force IgG
antibody response (good neutralizer)
Successful in reducing amount of Fel d 1 secretions. This was shown because the
percent of basophil activation went down.
If Fel D 1 was in secretions it should have activated basophils, and the reduction in
activated basophils demonstrated a reduction in Fel D 1. This proves that the vaccine
was successful in stimulating an immune response.
, *Combinatorial Diversity - correct Answer-created by somatic recombination of
randomly-selected gene segments
TCR alpha and BCR Light (very similar) - No D region
VJ C
Alpha: 70 V segments, 61 J segments = 4270 possible combinations
To make the TCR, one random alpha + one random beta chain (similar to BCR heavy
chain with VDJC) to make antigen binding site (1352X 4270 = 5.8 X 10^6 possible
combination) (still just starting with two genes, alpha and beta) -But this won't cover
enough (there are more than 6 million antigens, not even thinking about how many
different epitopes on each antigen)
*Diapedesis - correct Answer-As neutrophils go by they form weak connections
(temporarily binds and breaks free), but this slows the neutrophils down (keeps hitting
things and slowing down), starts tumbling - temporary attraction = Rolling adhesion -
then when neutrophil has slowed down more, an interaction that is much tighter occurs
and stops
Neutrophil starts to flatten out so it can squeeze through gaps into tissue space
(extravasation) - getting from inside the blood vessel to outside - DIAPEDESIS is the
way in which this happens/ Process of changing shapeChemokines: chemicals that are
at highest concentration near source of infection- kind of like trail of breadcrumbs-
cause intracellular changes that cause cell shape changes-Pus = dead neutrophils +
exudate
*For activation of T cells and formation of long-term memory, T cells require three
signals during antigen presentation. The three signals include - (signal 1) antigen
binding to the T cell receptor, (signal 2) <CHOOSE ANSWER> and (signal 3) cytokine
signaling from the APC and other innate cells. - correct Answer-co-stimulation by CD28
*B7 CD28: Used for Naive (found on APC)
CD28 is found on Th1 or Th2-cells
B7-CD28 interaction occurs when APC with antigen, presents to a T-cell to activate that
T-cell.
CD40L-CD40 interaction occurs when a helper T cell (CD-40L) activates a B-cell to
initiate class switching and antibody production.
*For variolation, the process of introducing a microbe or its antigens into a patient is
called: - correct Answer-Inoculation
The most common method was to use a needle to retrieve material from pustules from
a patient with variola minor and then stick the recipient in the arm with that needle.
*Granulocytes - correct Answer-Includes neutrophils, eosinophils, basophils, mast
cellsInnate immune cells that produce and respond to inflammatory signals.
-Second line of defense
