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J. Biol. Chem., Vol. 278, Issue 47, 46321-46328, November 21, 2003

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Characterization of Interferon- 13, a Novel Constitutive Murine Interferon- Subtype^*

Vincent van Pesch and Thomas Michiels

From the University of Louvain, Christian de Duve Institute of Cellular Pathology, Microbial Pathogenesis Unit, MIPA-VIRO 74-49, 74, avenue Hippocrate, B-1200, Brussels, Belgium

Type-I interferons (IFNs), also called IFNs-/, are a family of cytokines induced by viral infection and are primarily involved in antiviral defense of the cells. IFNs-/ were also reported to be produced constitutively at low levels in mouse and human cells. These so-called endogenous or constitutive IFNs are thought to exert important homeostatic functions in the uninfected host. By searching IFN genes that were not repressed by the leader protein of Theiler's virus, we identified three uncharacterized IFN- genes that are constitutively expressed in uninfected mouse cells, in vitro and in vivo. Two of these genes corresponded to pseudogenes and were tentatively called IFN-(2) and IFN-(3). IFN-(2) transcripts are the most abundant IFN- transcripts detected in several mouse organs in the absence of viral infection. The third gene codes for a new IFN- subtype called IFN-13, which exhibits acid-stable antiviral activity against Theiler's virus, Mengo virus, and vesicular stomatitis virus. IFN-13 displays unusual characteristics, suggesting that it might have a particular function. Firstly, it is transcribed constitutively, independent of viral infection and of interferon regulatory factor-7 induction. Secondly, it contains two N-glycosylation sites, in contrast to other murine IFN- subtypes that contain either one or no N-glycosylation site. In addition to the genes described here above, several other IFN- subtype genes, including a new gene (IFN-14), were expressed in tissues of uninfected mice. In contrast to IFN-13, IFN-14 was found to lack N-glycosylation and have its expression induced in response to viral infection.

Received for publication, March 13, 2003 , and in revised form, August 14, 2003.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBank^TM/EBI Data Bank with accession number(s) AY220461, AY220462, AY220463, AY220464, AY220465, BK001229, BK001230, AY226994, AY226995, AY226996, and AY226997.

^* This work was supported in part by convention 3.4549.02 of the FRSM, by the French Association pour la recherche sur la Sclérose en Plaques, and by the Fonds de Développement Scientifique of the University of Louvain. 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.

The on-line version of this article (available at http://www.jbc.org) contains Supplemental Tables A–C.

Research Fellow with the FNRS (Belgian National Fund for Scientific Research).

Research Associate with the FNRS. To whom correspondence should be addressed: University of Louvain, Christian de Duve Institute of Cellular Pathology, MIPA-VIRO 74-49, 74, avenue Hippocrate, B-1200, Brussels, Belgium. Tel.: 32-2-764-74-29; Fax: 32-2-764-74-95; E-mail: michiels{at}mipa.ucl.ac.be.

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