Document 0154 DOCN M9650154 TI Recombinant interferon-alpha selectively inhibits the production of interleukin-5 by human CD4+ T cells. DT 9605 AU Schandene L; Del Prete GF; Cogan E; Stordeur P; Crusiaux A; Kennes B; Romagnani S; Goldman M; Department of Immunology, Hopital Erasme-Cliniques; Universitaires de Bruxelles, Belgium. SO J Clin Invest. 1996 Jan 15;97(2):309-15. Unique Identifier : AIDSLINE MED/96149155 AB The effects of recombinant IFN-alpha on the production of IL-5 by human CD4+ T cells were first analyzed on resting CD4+ T cells purified from normal PBMC and stimulated either with a combination of PMA and anti-CD28 mAb or anti-CD3 mAb cross-linked on B7-1/CD32-transfected mouse fibroblasts. We found that IFN-alpha profoundly inhibited in a dose-dependent manner IL-5 production by resting CD4+ T cells whereas IL-10 was upregulated in both systems. The addition of a neutralizing anti-IL-10 mAb to PMA and anti-CD28 mAb upregulated IL-5 production by resting CD4+ T cells but did not prevent IFN-alpha-induced IL-5 inhibition. We then analyzed the effect of IFN-alpha on the production of cytokines by differentiated type 2 helper (Th2) CD4+CD3- cells isolated from peripheral blood of two patients with the hypereosinophilic syndrome. In both cases, IFN-alpha markedly inhibited IL-5 production while it induced mild upregulation of IL-4 and IL-10. Finally, the inhibitory effect of IFN-alpha on IL-5 production was confirmed on a panel of Th2 and Th0 clones generated in vitro. In 2 out of 6 clones, IL-5 inhibition was associated with upregulation of IL-4 and IL-10. We conclude that IFN-alpha selectively downregulates IL-5 synthesis by human CD4+ T cells. DE Animal Antigens, CD28/PHYSIOLOGY Base Sequence CD4-Positive T-Lymphocytes/*METABOLISM DNA Primers/CHEMISTRY Gene Expression Human Hypereosinophilic Syndrome/IMMUNOLOGY Interferon Alfa-2b/*PHARMACOLOGY Interleukin-10/BIOSYNTHESIS Interleukin-4/BIOSYNTHESIS Interleukin-5/*BIOSYNTHESIS Lymphocyte Transformation Mice Molecular Sequence Data Platelet Glycoprotein GPIIb-IIIa Complex/ANALYSIS RNA, Messenger/GENETICS Support, Non-U.S. Gov't Th2 Cells/*METABOLISM Transfection JOURNAL ARTICLE SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).