Fax +41 61 306 12 34 E-Mail karger@karger.ch www.karger.com Research Article J Innate Immun 2011;3:200–207 DOI: 10.1159/000321194 Induction of B Cell-Activating Factor by Viral Infection Is a General Phenomenon, but the Types of Viruses and Mechanisms Depend on Cell Type Marc Ittah   a Corinne Miceli-Richard   a Pierre Lebon   d Coralie Pallier   b Christine Lepajolec   c Xavier Mariette   a a  Service de Rhumatologie, Institut National de la Santé et la Recherche Médicale (INSERM) U 1012, Hôpital Bicêtre, Assistance Publique-Hôpitaux de Paris (AP-HP), Université Paris-Sud 11, et b  Service de Virologie et c  Service de Oto-rhino-laryngologie, Hôpital Bicêtre, AP-HP, Le Kremlin-Bicêtre, et d  Service de Virologie, Hôpital Cochin-Saint Vincent de Paul, AP-HP, Paris, France BAFF expression, but through a PKR-independent mecha- nism for these 3 cell types and a type 1 IFN-dependent mechanism in monocytes and SGECs. Thus, BAFF induction by viral infection is a general phenomenon, but the types of viruses and mechanisms of the induction depend on the cell type. Copyright © 2010 S. Karger AG, Basel Introduction B cell-activating factor of the TNF family (BAFF; also called BLyS) might explain autoimmune B cell activation in several systemic autoimmune diseases, including pri- mary Sjögren’s syndrome (pSS) [1], rheumatoid arthritis [2] and systemic lupus erythematosus (SLE) [3]. pSS is a prototype autoimmune disorder characterized by lym- phocytic infiltration of salivary and lachrymal glands leading to xerostomia and xerophtalmia. This disease fea- tures both local and systemic autoimmune B cell activa- tion mainly driven by BAFF. BAFF plays a crucial role in B cell maturation, plasma cell survival, antibody response and immunoglobulin class switch recombination [4]. In- terestingly, for not fully understood reasons, autoreactive B cells depend more on BAFF for survival than do allo- Key Words BAFF  Virus  Interferon  Autoimmunity  Innate immunity  Sjögren’s syndrome Abstract B cell-activating factor of the TNF family (BAFF) plays a key role in promoting B lymphocyte activation and survival. We previously showed in primary Sjögren’s syndrome that sali- vary gland epithelial cells (SGECs), the resident targeted cells of autoimmunity in this disease, can produce BAFF after in- fection with a double-stranded RNA (dsRNA) virus by a pro- tein kinase RNA (PKR)-dependent mechanism. This study aimed to assess the effect of different viruses on various cell types – SGECs but also dendritic cells (DCs) and mono- cytes – in the induction of BAFF. BAFF induction was ob- served after Sendai virus infection of monocytes and SGECs, as well as poly(I:C) stimulation of DCs. However, PKR inhibi- tion by 2-aminopurine failed to reduce BAFF expression in these infected or stimulated cells. Conversely, in Sendai vi- rus-infected monocytes, blocking type 1 interferon (IFN) re- ceptor by anti-IFNAR1 antibody strongly inhibited BAFF ex- pression. These results provide additional data suggesting that both dsRNA virus stimulation of DCs and single-strand- ed RNA virus infection of SGECs or monocytes can induce Received: July 19, 2010 Accepted after revision: September 15, 2010 Published online: November 3, 2010 Journal of Innate Immunity Prof. Xavier Mariette Service de Rhumatologie, Hôpital de Bicêtre 78 Rue du Général Leclerc FR–94275 Le Kremlin-Bicêtre (France) Tel. +33 1 4521 3758, Fax +33 1 4521 3757, E-Mail xavier.mariette  @  bct.ap-hop-paris.fr © 2010 S. Karger AG, Basel 1662–811X/11/0032–0200$38.00/0 Accessible online at: www.karger.com/jin