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?
What will be an ideal response?
Answer: The child did not have a reaction after the first bee sting because there was no immunoglobulin E specific for bee venom in the child's 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 cellâ€"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.
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