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Previous Volume 341:1112-1120 October 7, 1999 Number 15 Next

	Full Text PDF Editorial by Bain, B. J. Letters Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited Related Article PubMed Citation

ABSTRACT

Background The cause of persistent eosinophilia and the hypereosinophilic syndrome is unknown. Recent work suggests that in some patients with the hypereosinophilic syndrome, a clone of abnormal T cells produces large amounts of interleukin-5, a cytokine required for the growth and differentiation of eosinophils. We examined T-cell surface markers, rearranged T-cell–receptor genes, and in vitro production of cytokines by T cells from patients with 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 dominant (clonal) rearrangements of the T-cell receptor within the lymphocyte population, Southern blot analysis (ß chain) and the polymerase chain reaction ( 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 abnormal immunophenotype was unique. Evidence of clonal rearrangements of the T-cell receptor was obtained in 8 of the 16 patients. In most instances, the abnormal T cells expressed large amounts of surface proteins associated with T-cell activation (the chain of the interleukin-2 receptor and the HLA-DR antigen). Moreover, the aberrant T cells produced large amounts of interleukin-5 in vitro.

Conclusions Clonal populations of abnormal T cells producing interleukin-5 occur in some patients with idiopathic eosinophilia.

Source Information

From the Swiss Institute of Allergy and Asthma Research, University of Zurich, Davos, Switzerland (H.-U.S., K.B.); the Research Center for Environment and Health, Technical University of Munich, Munich, Germany (S.G.P.); and the Department of Dermatology, University of Zurich, Zurich, Switzerland (R.D.).

Address reprint requests to Dr. Simon at the Swiss Institute of Allergy and Asthma Research, University of Zurich, Obere Strasse 22, CH-7270 Davos, Switzerland, or at hus{at}siaf.unizh.ch.

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N Engl J Med 2000; 342:659-661, Mar 2, 2000. Correspondence

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