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allele in 13 of 20 patients with atopy, as compared with 5 of 30 control subjects.1 This mutation (termed Q576R) increases the signaling function of the interleukin-4 receptor, thereby favoring the expression of IgE receptors on immune cells.
We studied 75 patients with atopic dermatitis or asthma and 150 control subjects for the presence of the Q576R mutation. Wild-type and mutant alleles were amplified by the polymerase chain reaction with modified primers and segregated after enzymatic digestion with AvaI and electrophoretic migration. We
References
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