Host Defense Practice Exam 2
This is the practice exam sent out for the second Host Defense test.
- 1.
Which complement component and biological activity are incorrectly paired?
- A.
C9; membrane pore formation
- B.
C3b; pathogen opsonization
- C.
C3a; anaphylatoxin
- D.
C4a; binding to erythrocyte for IC removal
- E.
C5a; chemoattractant for leukocyte recruitment
Correct Answer
D. C4a; binding to erythrocyte for IC removalExplanation
C5a-9 all form the membrane attack complex that makes a membrane pore
C3b coats antigen (opsonization)
C3a, C4a, and C5a are all anaphylatoxins
C5a is a chemoattractant for neutrophils, eosinophils, basophils and monocytes (think "Chanel #5")Rate this question:
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- 2.
Which of the following would directly regulate formation of the membrane attack complex?
- A.
Factor H
- B.
Factor I & CD 46
- C.
CD 55
- D.
CD 59
- E.
C1 INH
Correct Answer
D. CD 59Explanation
CD59 prevents C8/9 association and pore assembly of MAC
Factor H, Factor I and CD46 all regulate C3b's C5 convertase activity
Factor I and CD46 regulate C4b's C3 convertase activity
CD55 regulates C3 convertase in all pathways by accelerating decay (think "55 raises speed-limit"
C1 INH, in classical pathway, dissociates C1r and C1s from C1qRate this question:
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- 3.
C3 and C5 convertases are involved in which pathway(s)?
- A.
Classical pathway only
- B.
MB-Lectin pathway only
- C.
Alternative pathway only
- D.
Both classical and MB-Lectin pathways
- E.
Classical, MB-Lectin and alternative pathways
Correct Answer
E. Classical, MB-Lectin and alternative pathwaysExplanation
All three pathways involve activity of C3 convertase and C5 convertaseRate this question:
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- 4.
A deficiency of complement component C1 would cause increased susceptibility to:
- A.
Immune complex disease
- B.
Bacterial infections, particularly in childhood
- C.
Infection by pyogenic bacteria and Neisseria spp.
- D.
Infection by Neisseria spp. only
- E.
Infection by pyogenic bacteria only
Correct Answer
A. Immune complex diseaseExplanation
lack of early classical components (C1, C2, C4) won't lead to overwhelming infection, but will decrease IC clearance and lead to IC diseaseRate this question:
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- 5.
Which of the following correctly describes IgA?
- A.
Serum IgA is primarily dimeric
- B.
Secreted mucosal IgA is mostly monomeric
- C.
The production of sIgA requires only the epithelial cells of the mucosa, not the plasma cell epithelium
- D.
SIgA contains a component of pIgR that is bound covalently
- E.
Dimeric IgA has no J chain
Correct Answer
D. SIgA contains a component of pIgR that is bound covalentlyExplanation
Serum IgA is mostly monomeric, while secretory IgA is mostly dimeric (joined by J chain). The production of sIgA requires plasma cells of lamina propria AND epithelial cells of mucosa.Rate this question:
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- 6.
When an antigen is consumed orally, the key feature that distinguishes the induction of a response and the induction of tolerance is...
- A.
Desensitization
- B.
Commensal bacterial development
- C.
Dendritic cell inactivation
- D.
Inflammation
- E.
Mucosal epithelium leakiness
Correct Answer
D. InflammationExplanation
When an antigen is consumed orally, the key feature that distinguishes the induction of a response and the induction of tolerance is inflammation. Inflammation is a natural response of the body to infection or injury, and it involves the release of various immune cells and molecules to fight against pathogens. In the case of consuming an antigen, if inflammation occurs, it indicates that the immune system is recognizing the antigen as a threat and will mount a response against it. On the other hand, if there is no inflammation, it suggests that the immune system is tolerating the antigen and not initiating a response.Rate this question:
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- 7.
Which of the following is not a symptom of selective IgA deficiency?
- A.
A family history of IgA deficiency of aggamaglobulinemia
- B.
A high incidence of oral infections
- C.
Frequency of respiratory infections
- D.
Chronic diarrhea
- E.
Subcutaneous mycoses in adulthood
Correct Answer
E. Subcutaneous mycoses in adulthoodExplanation
The correct answer is "Subcutaneous mycoses in adulthood". Selective IgA deficiency is a condition where the body lacks or produces very low levels of immunoglobulin A (IgA). This deficiency can result in various symptoms, including a family history of IgA deficiency or agammaglobulinemia, a high incidence of oral infections, frequency of respiratory infections, and chronic diarrhea. However, subcutaneous mycoses, which are fungal infections that affect the skin and underlying tissues, are not typically associated with selective IgA deficiency.Rate this question:
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- 8.
Commensal bacteria...
- A.
Promote the colonization of pathogenic bacteria in the guyt
- B.
Thrive with antibiotic treatment
- C.
Inhibit regulatory T cells
- D.
Are not involved in mucosal tolerance
- E.
Prevent the differentiation of immature dendritic cells to mature dendritic cells
Correct Answer
E. Prevent the differentiation of immature dendritic cells to mature dendritic cellsExplanation
Immature dendritic cells take up commensal bacteria, give weak signals to induce regulatory T-cell formation (inhibiting immune response and developing tolerance to the commensal bacteria). Destruction of commensal bacteria (eg. by antibiotics) allows pathogens (eg. clostridium difficile) to penetrate epithelial cells, bind to dendritic cells, make them mature and form immune response.Rate this question:
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- 9.
Onset of symptoms associated with X-linked Agammaglobulinemia develop later in infancy than problems associated with SCID. For X-linked Agammaglobulinemia, this is in part due to the mother's maternal Ab conferring immunity for 6-9 months post-partum. Why doesn't the maternal antibody help the SCID patients as much and why is the IgG pooled antibody administration not the preferred treatment choice for SCID patients?
- A.
Maternal antibody is inactivated in children with SCID; antibody administration is too risky
- B.
SCID involves a defect with both B & T cells; administering pooled antibodies does not solve the T-cell defect
- C.
SCID involves a defect with only T cells; administering pooled antibodies does not solve T-cell related defects
- D.
SCID patients have B-cells that are functional but they do not develop; administering pooled antibodies does not stimulate these faulty B-cells
- E.
Maternal antibody does help the SCID patients and IgG pooled antibody is the preferred treatment choice
Correct Answer
B. SCID involves a defect with both B & T cells; administering pooled antibodies does not solve the T-cell defectExplanation
The only treatment "routinely" available for SCID is bone marrow/stem cell transplantation.Rate this question:
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- 10.
Which of the following is NOT a characteristic of Common Variable Immunodeficiency (CVI)?
- A.
Patient has increased number of lymphocytes and produces abnormal IgG
- B.
Early B-cell development is normal but there is a marked reduction in terminal B-cells, plasma cells and reduced numbers of germinal centers
- C.
On an FACS analysis, you not normal or normal high levels of B-cells
- D.
CVI could involve inappropriate inhibition of B-cells by CD4, 25 FoxP3 cells
- E.
Defects may reside in defective cytokine signaling or cross-talk between B and Th2 cells
Correct Answer
A. Patient has increased number of lymphocytes and produces abnormal IgGExplanation
Patients with CVI have lots of B-cells, and no or very low IgG. The IgG itself is not abnormal; the levels are abnormally low. Terminal B-cell differentiation is defective, plasma cells do not form, and antibodies are not produced.
This is different from X-linked agammaglobulinemia, in which there is a defect in EARLY B-cell development and there are few or no B-cells present (therefore no plasma cells, no Ig of any kind)Rate this question:
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- 11.
Some SCID patients cannot be treated with a bone marrow transplant because they have no sibs that match and there is no donor in the registry who is an MHC match, so they are sometimes treated with gene transfer. What is the reason for a rare gamma-delta T-cell lymphoma found in SCID gene transfer patients?
- A.
The point of insertion of the viral vector leads to the lymphoma
- B.
The pathology of SCID leads to the lymphoma
- C.
A failed bone marrow transplant leads to the lymphoma
- D.
An uncontrolled TMMI response leads to the lymphoma
- E.
HLA antigen incompatibility leads to the lymphoma
Correct Answer
A. The point of insertion of the viral vector leads to the lymphomaExplanation
The rare gamma-delta T-cell lymphoma found in SCID gene transfer patients is caused by the point of insertion of the viral vector. When gene transfer is used as a treatment for SCID patients, a viral vector is used to insert the corrected gene into the patient's cells. However, in some cases, the point of insertion of the viral vector can disrupt the normal functioning of the cells and lead to the development of lymphoma.Rate this question:
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- 12.
Which of the following distinguishes an Arthus reaction from a normal inflammatory response?
- A.
Erythrocytes are needed to take excess IC to the liver for disposal
- B.
Activated neutrophils release IL-8
- C.
Preexisting antibodies complex with antigen
- D.
Antigen-antibody complexes interact with both FcR and CR1 on neutrophils
- E.
Painful inflammation results
Correct Answer
C. Preexisting antibodies complex with antigenExplanation
Arthus reactions are so large because a large amount of preexisting antibodies complex to form IC with the antigen. In a normal response, there's a delay in IC formation while B-cells produce antibody. In both situations, IC activates neutrophils via FcR and CR1. Activated neutrophils release IL-8 which recruits more neutrophils to the site. A painful inflammatory response occurs, and excess IC are carried to the liver bound to erythrocytes via CR1 receptors. In an Arthus reaction, CR1-medicated IC disposal is immediately overwhelmed.Rate this question:
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- 13.
What is the major way the body clears excess immune complexes?
- A.
They travel unbound in the blood to the liver.
- B.
They are bound to CR1 receptors on vascular endothelium and cause vascular inflammation
- C.
They travel bound to erythrocytes in the blood to the spleen
- D.
They travel in the circulation to the liver bound to CR1 receptors on blood cells
- E.
They are degraded at the site of inflammation
Correct Answer
D. They travel in the circulation to the liver bound to CR1 receptors on blood cellsExplanation
B, C and E are all true, but they are not the major clearance mechanisms.Rate this question:
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- 14.
Which is Type III hypersensitivity?
- A.
Systemic Lupus
- B.
Allergic Rhinitis
- C.
Goodpasture's Syndrome
- D.
A positive TB skin test
- E.
Grave's Disease
Correct Answer
A. Systemic LupusExplanation
Systemic Lupus - Type III, immune complex hypersensitivity (inability to properly dispose of IC)
Allergic Rhinitis - Type I, IgE mediated allergy
Goodpasture's Syndrome - Type II, auto-immunity to type IV collagen
A positive TB skin test - Type IV, TMMI -> granuloma
Grave's Disease - Type II, auto-antibodies to TSH receptor -> hyperthyroidismRate this question:
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- 15.
Choose the correct choice in each set of answers in the parentheses. How was the Rh problem solved?Maternal (APCs/B-cells) are inactivated by Rh specific (IgM/IgG) binding to (FcgRII/FcgRIII). The associated (ITAM/ITIM) signals the cell to stop (producing antibody/presenting antigen). This will protect the second Rh+ pregnancy.
Correct Answer
B-cells, IgG, FcgRII, ITIM, producing antibody Administering IgG "tricks" the woman's B-cells into thinking that they've already generated sufficient IgG. When Ig-Ag IC complexes bind to FcgRIII receptors on APCs, those cells are activated via ITAMs to phagocytize and present antigen. - 16.
Tregs regulate in all of the following ways except...
- A.
Competition
- B.
Inhibition via DCs
- C.
Secreting TGF-B
- D.
T-cell inhibition
- E.
Secreting INF-g
Correct Answer
E. Secreting INF-gExplanation
Tregs (regulatory T cells) play a crucial role in immune regulation by suppressing excessive immune responses. They achieve this through various mechanisms such as competition with other immune cells, inhibiting dendritic cells (DCs), secreting TGF-B (transforming growth factor-B), and inhibiting T-cell activation. However, Tregs do not secrete INF-g (interferon-gamma), which is a cytokine produced by other immune cells to enhance immune responses. Therefore, the correct answer is "Secreting INF-g."Rate this question:
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- 17.
Hyperacute rejection is characterized in all of the following ways except...
- A.
Is defined as accelerated rejection taking place within 48 hours of the transplantation
- B.
Arteriolar narrowing due to an increase in the thickness of the intima
- C.
Is mediated by recipient alloantibody directed against donor antigens that were present prior to transplantation
- D.
Transplantation of an A, B or AB organ into an "O" individual
- E.
Widespread vascular injury
Correct Answer
B. Arteriolar narrowing due to an increase in the thickness of the intimaExplanation
thickening of the intima occurs along with the fibrotic processes of chronic rejectionRate this question:
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- 18.
All of the following are examples of Host-versus-graft disease except
- A.
Hyperacute rejection
- B.
Bone marrow transplant
- C.
Acute rejection
- D.
Chronic rejection
- E.
Xenotransplant rejection
Correct Answer
B. Bone marrow transplantExplanation
Bone marrow transplant: graft-versus-host diseaseRate this question:
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- 19.
Which of the following statements is true:
- A.
The development of swelling, redness and throbbing pain in the patient's arm 8 hours after receiving a tetanus shot for the second time in a month is an example of acute hypersensitivity
- B.
If a patient develops Immune Complex disease, this is a definite sign that the patient has a bacterial infection
- C.
Peroxidase or immunoflorescent labelled anti-IgG, but not anti-C3b, are reagents used to identify ICs in a tissue biopsy
- D.
Binding of the IC to endothelial CR1 receptors results first in production of cytokines and next in attraction of neutrophils to the site of binding
- E.
None of the above
Correct Answer
D. Binding of the IC to endothelial CR1 receptors results first in production of cytokines and next in attraction of neutrophils to the site of bindingExplanation
A - due to HYPERacute hypersensitivity
B - patient developing IC disease may just be responding to immunization
C - Anti-C3b and anti-IgG are both used to identify ICs in tissue biopsiesRate this question:
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- 20.
Which of the following statements is true:
- A.
UVA light is especially influential in stimulating antigen presentation by dendritic cells of the skin
- B.
Postmenopausal women have a higher likelihood of developing autoimmune disorders due to their decreased estrogen levels
- C.
Patients with systemic immune complex disorders like SLE (systemic lupus erythomatus) often present with skin rashes, glomerular nephritis and joint pain
- D.
SLE is an example of Type II hypersensitivity
- E.
None of the above
Correct Answer
C. Patients with systemic immune complex disorders like SLE (systemic lupus erythomatus) often present with skin rashes, glomerular nephritis and joint painExplanation
A - UVB light (not UVA) stimulates antigen presentation
B - estogen increase likelihood of developing autoimmune disorders (likelihood is highest between puberty and menopause)
C - accumulation of ICs cause all of these problems (high FcR concentration in skin and kidney)
D - SLE is an example of Type III hypersensitivity (IC disease)Rate this question:
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- 21.
Which of the following statements is true:
- A.
In secondary immune responses the level of IgG in a patient's serum is always greater than the level of albumin
- B.
In SLE, the patient makes antibodies against proteins encoded in their DNA
- C.
Spleenomegaly develops as a result of the spleen's attempt to phagocytize the increased number of antibody-antigen complexes formed during IC disease
- D.
Serum from a patient with a chronic infection would have significantly increased levels of polyclonal IgE antibodies
- E.
None of the above
Correct Answer
E. None of the aboveExplanation
A - in secondary immune response, IgG level is elevated but is never higher than albumin level
B - in SLE, the patient makes antibodies against their actual DNA, not proteins encoded in their DNA
C - the spleen doesn't phagocytize the increased ICs formed during IC disease
D - Serum from a patient with a chronic infection would have increased polyclonal IgG (not IgE) antibodiesRate this question:
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- 22.
What type of hypersensitivity disease is Goodpasture's Syndrome?
- A.
Type I
- B.
Type II
- C.
Type III
- D.
Type IV
Correct Answer
B. Type IIExplanation
Auto-antibody (against type IV collagen in kidneys, lungs)
"prepared mind syndrome" - discovered that patient didn't produce type IV collagen because his tissues didn't cause reaction when exposed to Goodpasture serum (Goodpasture is atopic -- serum should cause the same problem when inserted into an unaffected individual)Rate this question:
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- 23.
Which of the following statements is true:
- A.
Serum sickness is an example of a systemic, rather than local, immune response
- B.
Persons with chronic infections usually have monoclonal hypergammaglobulinemia
- C.
Glomerular nephritis, thyroiditis, and juvenile rheumatoid arthritis result from Type I hypersensitivity responses
- D.
Platelets, but not fibrin, are found where an IC binds to FcgR on vascular endothelium
- E.
None of the above
Correct Answer
A. Serum sickness is an example of a systemic, rather than local, immune responseExplanation
B - polyclonal, not monoclonal ("frustrated" B-cells )
c - Type III, not Type I
d - both platelets and fibrin are found where an IC binds to FcgR on vascular endotheliumRate this question:
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- 24.
Which of the following properties is NOT shared by basophils and mast cells?
- A.
Both constitutively express high affinity Fce receptors
- B.
Both have cytoplasmic stores of vasoactive mediators
- C.
Both develop from hematopoietic precursors
- D.
Both reside in tissue sites
- E.
Both have cytoplasmic granules
Correct Answer
D. Both reside in tissue sitesExplanation
Basophils circulate; mast cells reside in tissue sitesRate this question:
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- 25.
Mast cells do NOT contain:
- A.
Histamine
- B.
Heparin
- C.
Thrombopoietin
- D.
GM-CSF
- E.
TNF-a
Correct Answer
C. ThrombopoietinExplanation
Mast cells don't contain thrombopoeitin, which would cause hematopoietic stem cells to form platelets and contribute to blood clotting. Mast cells do not promote clotting at all; they oppose it by secreting heparin.
Mast cells do contain histamine, heparin, GM-CSF and TNF-alphaRate this question:
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- 26.
The immediate reaction stage of an allergic reaction is characterized by
- A.
Infiltration by eosinophils, neutrophils and mast cells
- B.
Direct complement activation by trypase cleavage
- C.
Release of IL-3 and 5, and GM-CSF
- D.
Increase of FceR display
- E.
Eosinophil production of major basic protein and leukotrienes
Correct Answer
B. Direct complement activation by trypase cleavageExplanation
all other choices are associated with late responseRate this question:
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- 27.
Under the hyper-hygiene hypothesis, which of the following factors contributes to allergic hypersensitivity?
- A.
Increase in the number of childhood illnesses
- B.
Later exposure to acute childhood infections
- C.
Large families and/or early day care
- D.
Too much early exposure to environmental and infectious antigens
- E.
Over-production of T-regulator cells
Correct Answer
B. Later exposure to acute childhood infectionsExplanation
Early exposure to childhood illnesses may "set" normal Th1 and Th2 responses to subsequent environmental antigen exposure. Allergies are rarer in large families and with early day care. Lack of early exposure to infectious Ag and underproduction of Tregs are associated with risk of developing allergies.Rate this question:
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- 28.
Which of the following is not a reason why there is a wide disparity of symptoms experienced by a large population of humans after being infected with a virus?
- A.
Some individuals may have too few or mutated TLRs causing them to have no response to pathogen
- B.
Inherent polymorphism found at each level, including MHC, TLR, cytokines and DCs
- C.
Having the "wrong" TLR causing an ineffective or pathologic response
- D.
Having too many TLR creating a hyper-response and causing collateral damage
- E.
None of the above
Correct Answer
E. None of the aboveExplanation
The given answer is "none of the above" because all of the options listed are reasons why there is a wide disparity of symptoms experienced by a large population of humans after being infected with a virus. Some individuals may have too few or mutated TLRs, inherent polymorphism is found at each level including MHC, TLR, cytokines, and DCs, having the "wrong" TLR can cause an ineffective or pathologic response, and having too many TLRs can create a hyper-response and cause collateral damage. Therefore, none of the options can be excluded as a reason for the wide disparity of symptoms.Rate this question:
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- 29.
Choose the answer that best describes the role of an adjuvant in providing immunization.
- A.
An adjuvant is a peptide that is given to induce immunity to another peptide.
- B.
An adjuvant is a peptide that is hooked onto a polysaccharide antigen to help induce a T-dependent response to gain memory cells.
- C.
An adjuvant is a peptide that is hooked onto a polysaccharide antigen to help induce a NK-cell response to get rid of the antigen.
- D.
An adjuvant is a polysaccharide that is hooked onto a peptide antigen to help induce a T-dependent response to gain memory cells.
- E.
An adjuvant is a polysaccharide that is hooked onto a peptide antigen to help induce a NK-cell response to get rid of the antigen.
Correct Answer
B. An adjuvant is a peptide that is hooked onto a polysaccharide antigen to help induce a T-dependent response to gain memory cells.Explanation
An adjuvant is a substance that is added to a vaccine to enhance the immune response to the antigen. In this case, the adjuvant is described as a peptide that is attached to a polysaccharide antigen. The role of this adjuvant is to help induce a T-dependent response, which means it activates T cells to recognize and respond to the antigen. By doing so, it helps in the development of memory cells, which provide long-term immunity against the antigen.Rate this question:
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- 30.
In regards to the immune system failing during response to a tumor antigen, choose the correct event that takes place during this malfunction of the immune system.
- A.
NK cells not only kill tumor cells, but normally dividing cells as well.
- B.
B-cells lack the ability to differentiate to plasma cells and subsequently cannot make antibodies due to blockage of cytokine receptor by tumor cells.
- C.
Chemokines secreted by the tumor induce a Th0 cell to become a Treg cell, which provides protection for the tumor.
- D.
MHC-I or MHC-II is not able to present tumor peptide as foreign and therefore does not induce an immune response.
- E.
TLRs of the DCs do not recognize the tumor cells.
Correct Answer
C. Chemokines secreted by the tumor induce a Th0 cell to become a Treg cell, which provides protection for the tumor.Explanation
In this scenario, the malfunction of the immune system occurs when chemokines secreted by the tumor induce a Th0 cell to transform into a Treg cell. Treg cells are regulatory T cells that suppress the immune response, providing protection for the tumor. This malfunction allows the tumor to evade destruction by the immune system. The other options do not directly relate to the immune system failing during response to a tumor antigen.Rate this question:
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- 31.
Which of the following disease or afflictions has NOT been thought to be controlled by the use of monoclonal antibodies?
- A.
Rheumatoid Arthritis
- B.
Hashimoto's disease
- C.
Allergies
- D.
Transplantation rejection
- E.
B-cell antibody mediated diseases (B lymphoma)
Correct Answer
B. Hashimoto's diseaseExplanation
Monoclonal antibodies have been used to treat Rheumatoid Arthritis, Allergies, Transplantation rejection, and B-cell antibody mediated diseases (B lymphoma). However, Hashimoto's disease, an autoimmune disorder affecting the thyroid gland, has not been thought to be controlled by the use of monoclonal antibodies. Monoclonal antibodies are typically used to target specific proteins or cells involved in the disease process, and in the case of Hashimoto's disease, the underlying mechanism does not involve a specific protein or cell target that can be effectively treated with monoclonal antibodies.Rate this question:
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- 32.
Leprosy can induce a Th1 or Th2 response depending on (??). All of the following would be considered in a vaccine against leprosy except:
- A.
IL-12 genes
- B.
IL-12R genes
- C.
IL-10 genes
- D.
INF-g genes
- E.
Th1 TLR activation genes
Correct Answer
C. IL-10 genesExplanation
All of the others promote a Th1 response; don't want to suppress Th1 response with IL-10.Rate this question:
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- 33.
In order to combat diptheria toxin (extracellular toxin), you would do all of the following except...
- A.
Stimulate a Th2 response
- B.
Stimulate a Th1 response
- C.
Use the appropriate cytokines
- D.
Use IV anti-toxin IgG
- E.
Use an antigen that mimics the toxin
Correct Answer
B. Stimulate a Th1 responseExplanation
TMMI response will not help reduce the effects of the toxinsRate this question:
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- 34.
The genetic defect allowing infants to have BCG (intracellular pathogen) is most likely the result of:
- A.
IL-12
- B.
IL-10
- C.
IL-17
- D.
TGF-B
- E.
IL-4
Correct Answer
A. IL-12Explanation
need TMMI for intracellular pathogenRate this question:
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- 35.
Which of the following would be unhelpful in determining the antigen/antibody systems and antibody isotypes present in a patient's serum?
- A.
Ouchterlony test
- B.
Agar Gel Immunopreciptin assay
- C.
RAST
- D.
Skin test and serum tryptase
- E.
None of the above
Correct Answer
D. Skin test and serum tryptaseExplanation
Serum tryptase (measure of mast cell activation/degranulation) and skin tests are an INDIRECT measure of antigen/antibody system and antibody isotypes. Skin tests may be dangerous if the patient is highly reactive.Rate this question:
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- 36.
A patient is stung by a bee for the second time and develops urticaria, what isotype antibodies are being produce against the bee venom antigen and is this an appropriate immune response to bee venom?
- A.
Both IgE and IgG are produced, this is an appropriate immune responses to bee venom
- B.
Only IgE is produced, this is an appropriate response to bee venom
- C.
Both IgE and IgG are produced, this is an inappropriate immune responses to bee venom
- D.
Only IgG is produced, this is an inappropriate response to bee venom
- E.
Both IgE and IgA are produced, this is an appropriate response to bee venom
Correct Answer
C. Both IgE and IgG are produced, this is an inappropriate immune responses to bee venomExplanation
When a person is stung by a bee for the second time and develops urticaria, it indicates an allergic reaction. In this case, both IgE and IgG antibodies are being produced against the bee venom antigen. While IgE is the primary antibody involved in allergic reactions, the presence of IgG suggests a secondary immune response. This inappropriate immune response to bee venom can lead to symptoms such as urticaria.Rate this question:
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- 37.
Which of the following is an absolute requirement for an allergic reaction to occur?
- A.
IgG isotype switch
- B.
Armed basophils
- C.
IL-5 and eosinophils
- D.
Sensitization event
- E.
Low exposure to infectious agents as a child
Correct Answer
D. Sensitization eventExplanation
An allergic reaction occurs when the immune system becomes sensitized to a specific allergen. Sensitization refers to the initial exposure to the allergen, which triggers the production of specific IgE antibodies. These antibodies bind to mast cells and basophils, leading to their activation. When the allergen is encountered again, it binds to the IgE antibodies on mast cells and basophils, causing the release of inflammatory mediators such as histamine. This results in the symptoms of an allergic reaction. Therefore, a sensitization event is an absolute requirement for an allergic reaction to occur.Rate this question:
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- 38.
What are the effects of corticosteroids in an individual experiencing an allergic response and at what point do they act in the immune response?
- A.
Prevent anaphylaxis, early phase
- B.
Inhibit degranulation of IgE-armed mast cells and basophils, early reaction
- C.
Inhibit production of IL-4 and IL-13, late reaction
- D.
Suppress the production of IgE and enhance production of IgG, late reaction
- E.
Inhibit production of pro-inflammatory cytokines, late reaction
Correct Answer
E. Inhibit production of pro-inflammatory cytokines, late reactionExplanation
Corticosteroids act by inhibiting the production of pro-inflammatory cytokines during the late reaction of an allergic response. Pro-inflammatory cytokines are molecules that promote inflammation and immune responses. By inhibiting their production, corticosteroids help to reduce inflammation and alleviate symptoms associated with allergies. This action occurs during the late phase of the immune response, which is characterized by the release of cytokines and the recruitment of immune cells to the site of inflammation.Rate this question:
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- 39.
Which of the following is not characteristic of a Superantigen?
- A.
A superantigen does not bind to the conventional antigen binding site on MHC class II molecules
- B.
Superantigens are found in an unprocessed form between an MHC Class II and TCR
- C.
Superantigens can be responsible for septic shock and toxic shock syndrome via release of INF-gamma and massive release of TNF-alpha
- D.
A bacterial superantigen binds to the Beta chain on MHC class II molecule and the Alpha chain on the TCR
- E.
Superantigens can activate up to 20% of available CD4 cells
Correct Answer
D. A bacterial superantigen binds to the Beta chain on MHC class II molecule and the Alpha chain on the TCRExplanation
Bacterial superantigen binds to alpha chain on MHC class II and B chain on TCR.
Superantigens are found in unprocessed form; are not bound to conventional antigen-binding site.Rate this question:
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- 40.
Which of the following would not be a good example of a strategy used by a virus to evade the immune response?
- A.
Down-regulation of a TLR
- B.
Interference with MHC Class I and II antigen loading
- C.
Downregulate TGF-B in the vicinity of the pathogen
- D.
Increase IL-10 production in vicinity of the pathogen
- E.
Produce soluble cytokine receptors
Correct Answer
C. Downregulate TGF-B in the vicinity of the pathogenExplanation
Virus would induce CD4, 25 Tcell proliferation to block immune response against it, but by upregulating TGF-B. Viruses *do* produce soluble cytokine receptors.Rate this question:
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- 41.
- A.
TH1 cells producing IFN-gamma
- B.
TH17 cells producing IL-17
- C.
DC cells producing IL-12
- D.
GATA3 transcription factor
- E.
T-Bet transcription factor
Correct Answer
B. TH17 cells producing IL-17Explanation
T-cells at autoimmune sites are producing IL-17 (not INF-gamma). The transcription factor for Th17 is Ror. DCs at these sites produce IL-23 and IL-6, not IL-12. T-Bet is a Th1 transcription factor. GATA3 is a Th2 transcription factor.Rate this question:
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- 42.
Which of the following is an antigen-transporting cell?
- A.
Follicular Dendritic Cell
- B.
Langerhans Cell
- C.
Kupffer Cell
- D.
M Cell
- E.
B Cell
Correct Answer
D. M CellExplanation
M-cells transport antigens from the lumen of the GI tract and the bronchiolesRate this question:
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- 43.
Which one of these cells is probably not bone-marrow derived?
- A.
Th2 cell
- B.
Plasma Cell
- C.
Follicular Dendritic Cell
- D.
Macrophage
- E.
Eosinophil
Correct Answer
C. Follicular Dendritic CellExplanation
FDC is an antigen-retaining cell with Iccosomes on it; FDCs seem to be derived from reticular stromal cellsRate this question:
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- 44.
Which of the following is incorrectly matched?
- A.
Synapse I; location deep cortex, involves DC interacting with Th cell
- B.
Synapse II; Ag-activated Th cell interacting with Ag-activated B cell
- C.
Synapse III; B cell post-germinal center interacting with Th cell
- D.
CCL 19 and CCL 21 attract B cells to Dendritic Cells
- E.
All of the above are correct
Correct Answer
D. CCL 19 and CCL 21 attract B cells to Dendritic CellsExplanation
CCL19 and CCL21 attract T-cells, not B-cells.Rate this question:
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