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Previous Volume 330:535-538 February 24, 1994 Number 8 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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The hypereosinophilic syndrome is characterized by persistent eosinophilia of unknown origin often associated with the dysfunction of multiple organs as a result of tissue infiltration by eosinophils and the toxic effects of their products¹. Previous studies have suggested that T lymphocytes may be involved in the induction of the syndrome through the secretion of an eosinophil differentiation factor^2,3.

Helper T lymphocytes (CD4+ T cells) play a central part in normal and pathologic immune responses through the secretion of cytokines. Interleukin-2, interferon gamma, and tumor necrosis factor are involved in cell-mediated immunity, whereas interleukin-4 stimulates the production of IgE . . . [Full Text of this Article]

Case Report

Methods

Isolation of PBMC

Southern Blot Analysis of Gene Coding for the Chain of the T-Cell Receptor

Cell Cultures

Determination of Cytokine Levels in Serum and Culture Supernatants

Results

Analysis of Rearrangements of the Chain of the T-Cell-Receptor Gene

Profile of Cytokines Secreted by the CD4+CD3- T-Cell Clone

Effects of Methylprednisolone and Interferon Alfa-2b on Serum Interleukin-5 Levels

Discussion

Source Information

From the Department of Internal Medicine, Hopital Universitaire Brugmann (E.C.), the Department of Immunology, Hopital Universitaire Erasme (L.S., A.C., M.G.), and the Department of Medical Genetics, Institute of Interdisciplinary Research, Universite Libre de Bruxelles (P.C., T.V.) -- all in Brussels, Belgium.

Address reprint requests to Dr. Cogan at the Department of Internal Medicine, Hopital Universitaire Brugmann, 4, place Van Gehuchten, B 1020 Brussels, Belgium.

References

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