Alsharifi, M.Muellbacher, A.Regner, M.2014-11-242014-11-242008Immunology and Cell Biology, 2008; 86(3):239-2450818-96411440-1711http://hdl.handle.net/2440/87481The mammalian host responds to a microbial infection with a rapid innate immune reaction that is dominated by type I interferon (IFN-I) release. Most cells of vertebrates can respond to microbial attack with IFN-I production, but the cell type responsible for most of the systemic IFN-I release is thought to be plasmacytoid dendritic cells (pDCs). Besides its anti-microbial and especially anti-viral properties IFN-I also exerts a regulatory role on many facets of the sequential adaptive immune response. One of these is being the recently described partial, systemic activation of the vast majority of B and T lymphocytes in mice, irrespective of antigen reactivity. The biological significance of this partial activation of lymphocytes is at present speculative. Secondary infections occurring within a short time span of a primary infection fail to elicit a similar lymphocyte activation response due to a refractory period in systemic IFN-I production. This period of exhaustion in IFN-I responses is associated with an increased susceptibility of the host to secondary infections. The latter correlates with well-established clinical observations of heightened susceptibility of patients to secondary microbial infections after viral episodes.en© 2008 Australasian Society for Immunology Inc. All rights reserved.type I interferon; immunoregulation; viral infectionsJournal article003001329910.1038/sj.icb.71001590002544162000052-s2.0-4114912214196566