In delayed hypersensitivity, as the name implies, symptoms take a longer time (hours to days) to develop than in immediate hypersensitivity. This may be because immediate hypersensitiv-ity is mediated by antibodies, whereas delayed hypersensitivity is a cell-mediated T lymphocyte response. Since the symptoms are caused by the secretion of lymphokines rather than by the secretion of histamine, treatment with antihistamines provides little benefit. At present, corticosteroids are the only drugs that can effectively treat delayed hypersensitivity.
One of the best-known examples of delayed hypersensitivity is contact dermatitis, caused by poison ivy, poison oak, and poison sumac. The skin tests for tuberculosis—the tine test and the Mantoux test—also rely on delayed hypersensitivity reactions. If a person has been exposed to the tubercle bacillus and consequently has developed T cell clones, skin reactions appear within a few days after the tubercle antigens are rubbed into the skin with small needles (tine test) or are injected under the skin (Mantoux test).
Remember that Gary developed a rash on his abdomen the day following his time crawling through the underbrush in the hills. What may have caused Gary's rash? Why was it treated with cortisone rather than antihistamines?
Test Yourself Before You Continue
1. Explain the mechanisms that may be responsible for autoimmune diseases.
2. Distinguish between immediate and delayed hypersensitivity.
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