Blockade of interferon Beta, but not interferon alpha, signaling controls persistent viral infection.
Blockade of interferon Beta, but not interferon alpha, signaling controls persistent viral infection.
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DOI:
10.1016/j.chom.2015.04.005
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发表时间:
2015-05-13
影响因子:
30.3
通讯作者:
Oldstone MB
中科院分区:
文献类型:
--
作者:
Ng CT;Sullivan BM;Teijaro JR;Lee AM;Welch M;Rice S;Sheehan KC;Schreiber RD;Oldstone MB
Although type I interferon (IFN-I) is thought to be beneficial against microbial infections, persistent viral infections are characterized by high interferon signatures suggesting that IFN-I signaling may promote disease pathogenesis. During persistent lymphocytic choriomeningitis virus (LCMV) infection, IFNα and IFNβ are highly induced early after infection and blocking IFN-I receptor (IFNAR) signaling promotes virus clearance. We assessed the specific roles of IFNβ versus IFNα in controlling LCMV infection. While blockade of IFNβ alone does not alter early viral dissemination, it is important in determining lymphoid structure, lymphocyte migration, and anti-viral T cell responses that lead to accelerated virus clearance, approximating what occurs during attenuation of IFNAR signaling. Comparatively, blockade of IFNα was not associated with improved viral control but with early dissemination of virus. Thus, despite their use of the same receptor, IFNβ and IFNα have unique and distinguishable biologic functions, with IFNβ being mainly responsible for promoting viral persistence.
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DOI:
10.1073/pnas.1401662111
发表时间:
2014-05-20
影响因子:
11.1
作者:
Osokine, Ivan;Snell, Laura M.;Brooks, David
通讯作者:
Brooks, David
影响因子:
8.7
作者:
Piehler J;Thomas C;Garcia KC;Schreiber G
通讯作者:
Schreiber G
影响因子:
3.7
作者:
Oldstone MB;Campbell KP
通讯作者:
Campbell KP
影响因子:
5.4
作者:
BORROW, P;EVANS, CF;OLDSTONE, MBA
通讯作者:
OLDSTONE, MBA
影响因子:
11.2
作者:
Byrnes, AA;McArthur, JC;Karp, CL
通讯作者:
Karp, CL