INTERFERON-BETA IS REQUIRED FOR INTERFERON-ALPHA PRODUCTION IN MOUSE FIBROBLASTS

The type I interferons - interferon-alpha (IFN-alpha) and interferon-b eta (IFN-beta) - are critical for protection against viruses during th e acute stage of viral infection [1,2]. Furthermore, type I interferon s have been implicated as important mediators in the regulation of lym phocyte development [3], immune responses [4,5] and the maintenance of immunological memory of cytotoxic T cells [6,7]. The different IFN-al pha subtypes are encoded by 12 genes in the mouse [8] whereas IFN-beta is encoded by only one gene [9]. IFN-alpha and IFN-beta have a high d egree of sequence homology and are thought to interact with the same s urface receptor on target cells [10,11], As an approach to analysing t he different biological functions of IFN-alpha and IFN-beta, we have g enerated a mouse strain with an inactivated IFN-beta gene. We report h ere that embryonic fibroblasts from such mice produce neither IFN-beta nor IFN-alpha upon Sendai virus infection, whereas the production of IFN-alpha by leukocytes from the same strain of mice is intact, IFN-al pha production in embryonic fibroblasts from IFN-beta(-/-) mice could be rescued by 'priming' the cells using exogenous IFN-beta. These resu lts imply a unique role for IFN-beta in the induction of type I interf erons in peripheral tissues. (C) Current Biology Ltd.