Please use this identifier to cite or link to this item: https://doi.org/10.26508/lsa.201900298
Title: Viperin controls chikungunya virus-specific pathogenic T cell IFN? Th1 stimulation in mice
Authors: Carissimo, G.
Teo, T.-H.
Chan, Y.-H.
Lee, C.Y.-P.
Lee, B.
Torres-Ruesta, A.
Tan, J.J.L.
Chua, T.-K. 
Fong, S.-W. 
Lum, F.-M.
Ng, L.F.P. 
Issue Date: 2019
Publisher: Rockefeller University Press
Citation: Carissimo, G., Teo, T.-H., Chan, Y.-H., Lee, C.Y.-P., Lee, B., Torres-Ruesta, A., Tan, J.J.L., Chua, T.-K., Fong, S.-W., Lum, F.-M., Ng, L.F.P. (2019). Viperin controls chikungunya virus-specific pathogenic T cell IFN? Th1 stimulation in mice. Life Science Alliance 2 (1) : e201900298. ScholarBank@NUS Repository. https://doi.org/10.26508/lsa.201900298
Rights: Attribution 4.0 International
Abstract: Chikungunya virus (CHIKV) has been a worldwide threat since its reemergence in La Reunion Island in 2004. Expression of the interferon-stimulated protein Viperin correlates with viral load burden in patients, and studies in mice have demonstrated its role to limit disease severity against CHIKV infection. Using Viperin2/2 mice, we aimed to understand the contribution of Viperin to the T-cell immune response against CHIKV. CD4 T-cell depletion in Viperin2/2 mice showed that increased late acute joint inflammation (5-8 d postinfection) was exclusively mediated by T cells. Specifically, CHIKV-infected Viperin2/2 mice showed an increased INF? Th1 profile of CD4 T cells, enhanced INF? stimulation by APCs, an increased INF? secretion profile in the joint microenvironment, and increased numbers of inflammatory monocytes in virus-infected joints compared with WT mice. Bone marrow grafting experiments showed that Viperin expression in both hematopoietic and non-hematopoietic cells is instrumental in reducing disease severity associated with a CD4 T-cell response. © 2019 Carissimo et al.
Source Title: Life Science Alliance
URI: https://scholarbank.nus.edu.sg/handle/10635/210012
ISSN: 2575-1077
DOI: 10.26508/lsa.201900298
Rights: Attribution 4.0 International
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