Journal of Leukocyte Biology
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Originally published online as doi:10.1189/jlb.1003487 on February 24, 2004

Published online before print February 24, 2004
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(Journal of Leukocyte Biology. 2004;75:772-776.)
© 2004 by Society for Leukocyte Biology

Endothelial monocyte-activating polypeptide-II (EMAP-II): a novel inducer of lymphocyte apoptosis

J. C. Murray*,1, Y. M. Heng*, P. Symonds*, K. Rice*, W. Ward*, M. Huggins{dagger}, I. Todd{dagger} and R. A. Robins{dagger}

* Wolfson Digestive Diseases Centre, University Hospital, and
{dagger} Division of Immunology, School of Molecular Medical Sciences, University of Nottingham, United Kingdom

1 Correspondence: Wolfson Digestive Diseases Centre, University Hospital, University of Nottingham, Nottingham NG7 2UH, U.K. E-mail: cliff.murray{at}nott.ac.uk

The novel, proinflammatory cytokine endothelial monocyte-activating polypeptide-II (EMAP-II) was first found in tumor cell supernatants. EMAP-II is closely related or identical to the p43 auxiliary protein of the multisynthase complex, which is involved in protein synthesis. In vitro, EMAP-II induces procoagulant activity, increased expression of E- and P-selectins and tumor necrosis factor receptor-1, and ultimately, programmed cell death (apoptosis) in cultured endothelial cells. EMAP-II is also chemotactic for monocytes and neutrophils. However, the role of the p43/EMAP-II cytokine form in tumors is not understood. We hypothesized an immune-regulatory role within neoplastic tissues and investigated its effects on lymphocytes. EMAP-II causes a dose-dependent inhibition of proliferation and apoptosis in Jurkat T cells and mitogen-activated peripheral blood mononuclear cells. Coculture with DLD-1 colorectal cancer cells or media conditioned by these cells induces apoptosis in Jurkat cells, which is partially reversed by antibodies against EMAP-II. Our data suggest that EMAP-II constitutes a component of a novel, immunosuppressive pathway in solid tumors, which is not normally expressed outside the cell but in tumors, may be subject to abnormal processing and released from tumor cells.

Key Words: cytokine • tumor • p43 • immune evasion




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