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Herpesvirus Entry Mediator-Ig Treatment during Immunization Aggravates Rheumatoid Arthritis in the Collagen-Induced Arthritis Model¹

Matthias Pierer^2,*, Anett Schulz^*, Manuela Rossol^*, Eva Kendzia^*, Diego Kyburz, Holm Haentzschel^*, Christoph Baerwald^* and Ulf Wagner^*

^* Medical Department I, Department of Rheumatology, University of Leipzig, Leipzig, Germany; and Center of Experimental Rheumatology, Department of Rheumatology, and Center of Integrative Human Physiology, University of Zurich, Zurich, Switzerland

Previous studies attempting to influence the severity of collagen-induced arthritis (CIA) by modulating the LIGHT (lymphotoxin-related inducible ligand that competes for glycoprotein D binding to herpesvirus entry mediator (HVEM) on T cells)/lymphotoxin pathway have yielded conflicting results. To further clarify the role of LIGHT in autoimmune arthritis, a HVEM-Ig fusion protein was used. CIA was induced in DBA1 mice, which were injected i.p. with recombinant HVEM-Ig fusion protein and control Ig at different time points. Severity of clinical arthritis and histologic joint destruction were significantly increased in HVEM-Ig-treated mice compared with control-Ig-treated mice. Collagen II-induced in vitro T cell proliferation and IFN- production was augmented in mice treated with HVEM-Ig, as was the production of IgG2a anti-collagen II Ab. Accordingly, serum concentrations of IFN- and IL-6 were higher in mice treated with HVEM-Ig. In conclusion, HVEM-Ig aggravates autoimmunity in collagen-induced arthritis, which is possibly mediated by interaction with B and T lymphocyte attenuator (BTLA) or CD160, despite the blockade of LIGHT. Hence, HVEM-Ig seems not to be a valid therapeutic option in autoimmune arthritis.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Grant Pi 624/1-2 from the Deutsche Forschungsgemeinschaft (DFG).

² Address correspondence and reprint requests to Dr. Matthias Pierer, Department of Rheumatology, University of Leipzig, Max-Bürger Forschungszentrum, 04103 Leipzig, Germany. E-mail address: matthias.pierer{at}medizin.uni-leipzig.de

³ Abbreviations used in this paper: LIGHT, lymphotoxin-related inducible ligand that competes for glycoprotein D binding to herpesvirus entry mediator on T cells; BTLA, B and T lymphocyte attenuator; CIA, collagen-induced arthritis; CII, type II collagen; HVEM, herpesvirus entry mediator; LT, lymphotoxin.

⁴ The online version of this article contains supplemental material.