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https://hdl.handle.net/2440/87481
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Type: | Journal article |
Title: | Interferon type I responses in primary and secondary infections |
Author: | Alsharifi, M. Muellbacher, A. Regner, M. |
Citation: | Immunology and Cell Biology, 2008; 86(3):239-245 |
Publisher: | Nature Publishing Group |
Issue Date: | 2008 |
ISSN: | 0818-9641 1440-1711 |
Statement of Responsibility: | Mohammed Alsharifi, Arno Müllbacher and Matthias Regner |
Abstract: | 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. |
Keywords: | type I interferon; immunoregulation; viral infections |
Rights: | © 2008 Australasian Society for Immunology Inc. All rights reserved. |
DOI: | 10.1038/sj.icb.7100159 |
Published version: | http://dx.doi.org/10.1038/sj.icb.7100159 |
Appears in Collections: | Aurora harvest 7 Molecular and Biomedical Science publications |
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