Exam 27: Adaptive Immunity: Highly Specific Host Defenses
A child is stung by a bee at the beginning of the summer and has mild swelling and itching at the site of the sting. In late summer, the child is stung again, but this time rapidly develops anaphylaxis and is diagnosed with type I hypersensitivity to bee venom. If the child is allergic to bee venom, why was there no reaction after the first bee sting? What specifically happened after the first sting that led to the allergic reaction?
The child did not have a reaction after the first bee sting because there was no immunoglobulin E specific for bee venom in the childʹs blood or tissues yet. After the first bee sting, mucosa-associated B cells and TH2 cells produced cytokines that induce B cells to make IgE antibodies against the bee venom. Rather than circulating like IgG or IgM, the allergen-specific IgE antibodies bind to IgE receptors on mast cells. Mast cells are nonmotile granulocytes associated with the connective tissue adjacent to capillaries throughout the body. With any subsequent exposure to the immunizing allergen, the mast cell-bound IgE molecules bind the antigen. Cross-linking of IgEs by an antigen triggers the release of soluble allergic mediators from the mast cells, a process called degranulation. These mediators cause allergic symptoms within minutes of antigen exposure. After initial sensitization by an allergen, the allergic child will respond to each subsequent exposure to the allergen. Therefore, only after the second bee sting did the child show the signs of type I hypersensitivity or anaphylaxis. The first bee sting sensitized the child to the venom.
In class switching during the secondary antibody response, the most common antibody switch is from
C
The major histocompatibility complex in humans is also called the
A
Antihistamines are used to treat some allergic symptoms because they neutralize the histamine mediators that cause rapid dilation of blood vessels and contraction of smooth muscles that initiate the symptoms of systemic anaphylaxis.
What role does the C domain play in cell surface proteins that interact directly with antigens?
Which of the treatments listed below would be most effective for a patient with a genetic defect that causes severe combined immunodeficiency (SCID), a condition in which there is a severe deficiency in B and T lymphocytes?
You are bitten by a venomous snake at a nature center. You are rushed to the emergency room and given an antiserum. The snake handler says that he was bitten previously, but did not need treatment because he said he was exposed to venom so many times that he is immune. What is antiserum and will you have long-lasting immunity to snake venom after this? If the snake handler has truly developed some level of immunity, then how has that happened?
Which of the following is secreted by Th1 cells to stimulate macrophage differentiation and activation?
TCRs recognize epitopes only after the immunogens have been partially degraded.
CD4 and CD8 proteins are used for in vitro tests as T cell markers to differentiate TH cells from TC cells.
More than ________% of all T cell precursors that enter the thymus do NOT survive the selection process.
Which of the following enzymes are NOT secreted by TH1 to activate macrophages?
Some immature B cells are reactive to self-antigens but do not become activated even when exposed to high concentrations of self-antigens.
Given that T cell receptors (TCRs) are randomly generated during the maturation process, how are new T cells selected that can recognize self-antigens and other immune cells appropriately?
Which is an example of acquisition of natural passive immunity?
Proteins derived from infecting viruses are taken up and digested in the cytoplasm in a structure called the
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