The Journal of Experimental Medicine
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Published 16 September 2002. doi:10.1084/jem.20020319
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© Rockefeller University Press, 0022-1007/2002/9/829/ $5.00
The Journal of Experimental Medicine, Volume 196, Number 6, September 16, 2002 829-839

Inhibition of Type 1 Cytokine–mediated Inflammation by a Soluble CD30 Homologue Encoded by Ectromelia (Mousepox) Virus

Margarida Saraiva1, Philip Smith2, Padraic G. Fallon2 and Antonio Alcami1

1 Division of Virology, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, United Kingdom
2 Division of Microbiology and Parasitology, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, United Kingdom

Address correspondence to Antonio Alcami, Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Level 5, Box 157, Hills Road, Cambridge CB2 2QQ, United Kingdom. Phone: 44-1223-763403; Fax: 44-1223-330158; E-mail: aa258{at}mole.bio.cam.ac.uk

CD30 is up-regulated in several human diseases and viral infections but its role in immune regulation is poorly understood. Here, we report the expression of a functional soluble CD30 homologue, viral CD30 (vCD30), encoded by ectromelia (mousepox) virus, a poxvirus that causes a severe disease related to human smallpox. We show that vCD30 is a 12-kD secreted protein that not only binds CD30L with high affinity and prevents its interaction with CD30, but it also induces reverse signaling in cells expressing CD30L. vCD30 blocked the generation of interferon {gamma}–producing cells in vitro and was a potent inhibitor of T helper cell (Th)1- but not Th2-mediated inflammation in vivo. The finding of a CD30 homologue encoded by ectromelia virus suggests a role for CD30 in antiviral defense. Characterization of the immunological properties of vCD30 has uncovered a role of CD30–CD30L interactions in the generation of inflammatory responses.

Key Words: poxviruses • immunomodulation • cytokine • TNFR superfamily • Th-1


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