Background The cause of persistent eosinophilia and the hypereosinophilic s
yndrome is unknown. Recent work suggests that in some patients with the hyp
ereosinophilic syndrome, a clone of abnormal T cells produces large amounts
of interleukin-5, a cytokine required for the growth and differentiation o
f eosinophils. We examined T-cell surface markers, rearranged T-cell-recept
or genes, and in vitro production of cytokines by T cells from patients wit
h idiopathic eosinophilia.
Methods The expression of surface molecules on T cells was measured by flow
cytometry. Cytokine expression was measured by enzyme-linked immunosorbent
assay, flow cytometry, and immunohistochemical analysis. To identify domin
ant (clonal) rearrangements of the T-cell receptor within the lymphocyte po
pulation, Southern blot analysis (beta chain) and the polymerase chain reac
tion (gamma chain) were performed according to standard protocols.
Results Among 60 patients with idiopathic eosinophilia, 16 had circulating
T cells with an aberrant immunophenotype. In each of these patients, the ab
normal immunophenotype was unique. Evidence of clonal rearrangements of the
T-cell receptor was obtained in 8 of the 16 patients. In most instances, t
he abnormal T cells expressed large amounts of surface proteins associated
with T-cell activation (the a chain of the interleukin-2 receptor and the H
LA-DR antigen). Moreover, the aberrant T cells produced large amounts of in
terleukin-5 in vitro.
Conclusions Clonal populations of abnormal T cells producing interleukin-5
occur in some patients with idiopathic eosinophilia. (N Engl J Med 1999;341
:1112-20.) (C)1999, Massachusetts Medical Society.