T-cell clonality, as identified by T-cell receptor (TCR) gene rearrangements, has been identified in the lymphocytic variant of the hypereosinophilic syndrome (L-HES) (1, 2). Monoclonal T cells in L-HES exhibit an aberrant cell surface immu-nophenotype and produce increased amount of the Th2 cytokine interleukin-5 (IL-5). In eosinophilic disorders limited to one organ, studies are lacking to determine whether such abnormal circulating T cells may similarly promote the expansion of the eosinophilic cell lineage.
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