Link to Pubmed [PMID] – 21051868
J Innate Immun 2011;3(2):200-7
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 salivary gland epithelial cells (SGECs), the resident targeted cells of autoimmunity in this disease, can produce BAFF after infection with a double-stranded RNA (dsRNA) virus by a protein 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 monocytes – in the induction of BAFF. BAFF induction was observed after Sendai virus infection of monocytes and SGECs, as well as poly(I:C) stimulation of DCs. However, PKR inhibition by 2-aminopurine failed to reduce BAFF expression in these infected or stimulated cells. Conversely, in Sendai virus-infected monocytes, blocking type 1 interferon (IFN) receptor by anti-IFNAR1 antibody strongly inhibited BAFF expression. These results provide additional data suggesting that both dsRNA virus stimulation of DCs and single-stranded RNA virus infection of SGECs or monocytes can induce BAFF expression, but through a PKR-independent mechanism 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.