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Cytokine. 2001 Jun 7;14(5):272-82.

IFN-beta inhibits the ability of T lymphocytes to induce TNF-alpha and IL-1beta production in monocytes upon direct cell-cell contact.

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Division of Immunology and Allergy, Clinical Immunology Unit (Hans Wilsdorf Laboratory), Department of Internal Medicine, University Hospital, Geneva, Switzerland.


Tumour necrosis factor (TNF)-alpha and interleukin (IL-)1beta, essential players in the pathogenesis of immuno-inflammatory diseases, are strongly induced in monocytes by direct contact with stimulated T lymphocytes. The present study shows that the latter mechanism is inhibited by interferon (IFN)-beta. In co-cultures of autologous T lymphocytes and monocytes stimulated by phytohaemagglutinin (PHA), IFN-beta inhibited the production of TNF-alpha and IL-1beta by 88 and 98%, respectively, whereas the simultaneous production of IL-1 receptor antagonist (IL-1Ra), was enhanced two-fold. The latter effects of IFN-beta were independent of modulations in IFN-gamma, IL-4 and IL-10 production. When monocytes were activated by plasma membranes of stimulated T cells, IFN-beta slightly inhibited the production of TNF-alpha and IL-1beta, while enhancing 1.5-fold that of IL-1Ra. The latter effect correlated with the persistence of high steady-state levels of IL-1Ra mRNA after 24 h of activation. Membranes isolated from T lymphocytes that had been stimulated in the presence of IFN-beta displayed a 80% decrease in their capacity to induce the production of IL-1beta and TNF-alpha in monocytes, whereas IL-1Ra induction was decreased by only 32%. These results demonstrate that IFN-beta modulates contact-mediated activation of monocytes by acting on both T lymphocytes and monocytes, decreasing the ability of T lymphocytes to induce TNF-alpha and IL-1beta production in monocytes and directly enhancing the production of IL-1Ra in the latter cells.

[Indexed for MEDLINE]

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