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The type I interferons--interferon-alpha (IFN-alpha) and interferon-beta (IFN-beta)--are critical for protection against viruses during the acute stage of viral infection [1,2]. Furthermore, type I interferons have been implicated as important mediators in the regulation of lymphocyte development [3], immune responses [4,5] and the maintenance of immunological memory of cytotoxic T cells [6,7]. The different IFN-alpha 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 degree of sequence homology and are thought to interact with the same surface receptor on target cells [10,11]. As an approach to analysing the different biological functions of IFN-alpha and IFN-beta, we have generated a mouse strain with an inactivated IFN-beta gene. We report here that embryonic fibroblasts from such mice produce neither IFN-beta nor IFN-alpha upon Sendal virus infection, whereas the production of IFN-alpha by leukocytes from the same strain of mice is intact. IFN-alpha production in embryonic fibroblasts from IFN-beta-/- mice could be rescued by 'priming' the cells using exogenous IFN-beta. These results imply a unique role for IFN-beta in the induction of type I interferons in peripheral tissues.
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R Blumenthal, and
M L Eloranta, and
H Engel, and
G Alm, and
S Weiss, and
T Leanderson
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T Leanderson
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L Erlandsson, and
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M L Eloranta, and
H Engel, and
G Alm, and
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T Leanderson
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T Leanderson
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L Erlandsson, and
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L Erlandsson, and
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L Erlandsson, and
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T Leanderson
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L Erlandsson, and
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G Alm, and
S Weiss, and
T Leanderson
June 2016,
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L Erlandsson, and
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M L Eloranta, and
H Engel, and
G Alm, and
S Weiss, and
T Leanderson
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