Allergy and Hypersensitivity Flashcards
Upon initial exposure to allergen, plasma cells secrete antigen-specific IgE that binds to mast cell FceRI. The mast cells are said to be
a. activated.
b. allergenic.
c. anaphylactic.
d. sensitized.
e. tolerized.
d. sensitized.
An immediate allergic mediator released by mast cells is
a. epinephrine.
b. IgE.
c. IL-4.
d. histamine.
e. prostaglandin.
d. histamine.
Humans probably make IgE responses because
a. IgE binds more efficiently to low doses of antigen than IgG
b. IgE is protective against dangerous pollens.
c. IgE triggers eosinophils to release products toxic to helminth parasites
d. their T cells were not properly tolerized to self IgE in the thymus.
e. they cannot produce enough IgG to protect themselves against allergens.
c. IgE triggers eosinophils to release products toxic to helminth parasites
All of the following are Type I hypersensitivities EXCEPT
a. an allergy to peanuts.
b. an anaphylactic reaction to bee stings.
c. a blood transfusion reaction.
d. asthma induced by cat dander.
e. hay fever.
c. a blood transfusion reaction.
Fran walks outside on a beautiful day and takes a deep breath of ragweed pollen, to which she has a strong Type I hypersensitivity. Which event below will NOT occur within 30 minutes due to this hypersensitivity?
a. A local inflammatory response in the nose is induced, resulting in a runny or stuffy nose.
b. IgE specific for ragweed pollen is synthesized by B cells in the local lymph nodes.
c. Mast cells respond to the antigen-IgE signal by releasing preformed histamine
d. Ragweed pollen antigen binds to IgE present on mast cell FceRI in the respiratory tract.
e. Systemic effects of hypersensitivity such as anaphylactic shock may occur.
b. IgE specific for ragweed pollen is synthesized by B cells in the local lymph nodes.
Type II hypersensitivities involve
a. anaphylactic shock.
b. complement-mediated lysis of antibody-coated cells.
c. cytotoxic T cell mediated lysis of antibody coated cells
d. chemotaxis of eosinophils.
e. IgE-mediated degranulation of mast cells.
b. complement-mediated lysis of antibody-coated cells.
All of the following are Type II hypersensitivities EXCEPT
a. a blood transfusion reaction to AB antigens on erythrocytes.
b. autoimmune hemolytic anemia, production of autoantibodies to erythrocyte antigens.
c. drug-induced hemolytic anemia, production of antibodies to medications which can bind to erythrocytes.
d. Grave’s disease, production of autoantibodies to TSH receptor on thyroid cells.
e. serum sickness, production of antibodies to passively administered foreign antibodies.
e. serum sickness, production of antibodies to passively administered foreign antibodies.
Type II hypersensitivity results in all of the following EXCEPT
a. attraction and activation of inflammatory cells.
b. increased vascular permeability.
c. lysis of antibody coated cells by NK cells.
d. mediator release by CTL.
e. release of cytokines by macrophages.
d. mediator release by CTL.
A Type III hypersensitivity reaction is mediated by
a. antibody reacting with membrane antigen epitopes.
b. autoimmune reactions to self tissue antigens.
c. complement activation by immune complexes deposited in the blood vessel walls, kidneys, and joints.
d. cytokine release by Th1 cells.
e. the cell-mediated branch of the immune system.
c. complement activation by immune complexes deposited in the blood vessel walls, kidneys, and joints.
As he cleared brush near his home, Frank was bitten by a rattlesnake. He went to the emergency room for treatment with horse IgG anti-rattlesnake venom. About a week after the treatment, Frank experienced a rash, fever, swollen lymph nodes, and pains in his joints, all symptoms of serum sickness. These symptoms are probably due to
a. a T cell memory response to horse IgG.
b. cross reactivity between horse IgG and human IgG.
c. late phase damage caused by the rattlesnake venom
d. production of IgG anti-horse immunoglobulin, which triggered a Type III hypersensitivity.
e. production of IgG anti-rattlesnake venom, which triggered a Type III hypersensitivity.
d. production of IgG anti-horse immunoglobulin, which triggered a Type III hypersensitivity.
In the situation described in Question 10 above, Frank can be treated with
a. antiserum to complement to block its activation.
b. human anti-horse IgG to more quickly clear the horse antibody.
c. immunosuppressive drugs to block B cell production of antibody.
d. plasmapheresis to remove antigen-antibody complexes from the blood.
e. rattlesnake venom to absorb the horse anti-venom antibody.
d. plasmapheresis to remove antigen-antibody complexes from the blood.
Type IV hypersensitivity (DTH)
a. can be passively transferred with CD4 T cells.
b. causes chicken pox.
c. involves cell damage induced by IgG antibodies which are produced late in an immune response.
d. is mediated by memory macrophages.
e. occurs 1-2 weeks after antigen exposure.
a. can be passively transferred with CD4 T cells.
During Delayed Type Hypersensitivity reactions, macrophages
a. are not antigen specific.
b. are stimulated by IFN.
c. do not depend on antibody for antigen recognition.
d. kill neighboring cells, whether infected or not.
e. all of the above are true.
e. all of the above are true.
A positive skin reaction to tuberculin means that one has
a. an active case of tuberculosis.
b. an allergy to Mycobacterium tuberculosis.
c. antibodies specific for M. tuberculosis.
d. macrophages containing M. tuberculosis in their phagolysosomes.
e. memory CD4 T cells specific for M. tuberculosis.
e. memory CD4 T cells specific for M. tuberculosis.
A common feature of all hypersensitivities is
a. activation of CTL.
b. activation of Th2 cells.
c. antibody synthesis.
d. inflammation.
e. all of the above.
d. inflammation.
