Interferon type I responses in primary and secondary infections.
The 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.
Alsharifi
Mohammed
M
Division of Immunology and Genetics, The John Curtin School of Medical Research, Australian National University, Canberra, Australian Capital Territory, Australia. mohammed.alsharifi@anu.edu.au
Müllbacher
Arno
A
Regner
Matthias
M
D000818:Animals; D003713:Dendritic Cells / Q000378:metabolism / Q000473:pathology; D004198:Disease Susceptibility; D006801:Humans; D007110:Immunity, Active; D007113:Immunity, Innate; D007156:Immunologic Memory; D007239:Infections / Q000276:immunology / Q000503:physiopathology*; D007370:Interferon Type I / Q000276:immunology / Q000378:metabolism; D008213:Lymphocyte Activation
D007370:Interferon Type I