scholarly journals STAT2 dependent Type I Interferon response promotes dysbiosis and luminal expansion of the enteric pathogen Salmonella Typhimurium

2019 ◽  
Vol 15 (4) ◽  
pp. e1007745 ◽  
Author(s):  
R. Paul Wilson ◽  
Sarah A. Tursi ◽  
Glenn J. Rapsinski ◽  
Nicole J. Medeiros ◽  
Long S. Le ◽  
...  
2020 ◽  
Vol 34 (3) ◽  
pp. 4329-4347 ◽  
Author(s):  
Sabira Mohammed ◽  
Nalanda S. Vineetha ◽  
Shirley James ◽  
Jayasekharan S. Aparna ◽  
Manendra Babu Lankadasari ◽  
...  

Cell Reports ◽  
2017 ◽  
Vol 18 (10) ◽  
pp. 2373-2386 ◽  
Author(s):  
Abdul S. Qadir ◽  
Paolo Ceppi ◽  
Sonia Brockway ◽  
Calvin Law ◽  
Liang Mu ◽  
...  

2007 ◽  
Vol 283 (2) ◽  
pp. 802-808 ◽  
Author(s):  
Gagik Oganesyan ◽  
Supriya K. Saha ◽  
Eric M. Pietras ◽  
Beichu Guo ◽  
Andrea K. Miyahira ◽  
...  

2020 ◽  
Vol 117 (32) ◽  
pp. 19475-19486
Author(s):  
Carina Elsner ◽  
Aparna Ponnurangam ◽  
Julia Kazmierski ◽  
Thomas Zillinger ◽  
Jenny Jansen ◽  
...  

The DNA sensor cGAS catalyzes the production of the cyclic dinucleotide cGAMP, resulting in type I interferon responses. We addressed the functionality of cGAS-mediated DNA sensing in human and murine T cells. Activated primary CD4+T cells expressed cGAS and responded to plasmid DNA by upregulation of ISGs and release of bioactive interferon. In mouse T cells, cGAS KO ablated sensing of plasmid DNA, and TREX1 KO enabled cells to sense short immunostimulatory DNA. Expression ofIFIT1andMX2was downregulated and upregulated in cGAS KO and TREX1 KO T cell lines, respectively, compared to parental cells. Despite their intact cGAS sensing pathway, human CD4+T cells failed to mount a reverse transcriptase (RT) inhibitor-sensitive immune response following HIV-1 infection. In contrast, infection of human T cells with HSV-1 that is functionally deficient for the cGAS antagonist pUL41 (HSV-1ΔUL41N) resulted in a cGAS-dependent type I interferon response. In accordance with our results in primary CD4+T cells, plasmid challenge or HSV-1ΔUL41N inoculation of T cell lines provoked an entirely cGAS-dependent type I interferon response, including IRF3 phosphorylation and expression of ISGs. In contrast, no RT-dependent interferon response was detected following transduction of T cell lines with VSV-G-pseudotyped lentiviral or gammaretroviral particles. Together, T cells are capable to raise a cGAS-dependent cell-intrinsic response to both plasmid DNA challenge or inoculation with HSV-1ΔUL41N. However, HIV-1 infection does not appear to trigger cGAS-mediated sensing of viral DNA in T cells, possibly by revealing viral DNA of insufficient quantity, length, and/or accessibility to cGAS.


2008 ◽  
Vol 9 (4) ◽  
pp. 378-387 ◽  
Author(s):  
Anna Yarilina ◽  
Kyung-Hyun Park-Min ◽  
Taras Antoniv ◽  
Xiaoyu Hu ◽  
Lionel B Ivashkiv

Neuron ◽  
2017 ◽  
Vol 96 (6) ◽  
pp. 1290-1302.e6 ◽  
Author(s):  
Vidhu Mathur ◽  
Ritwik Burai ◽  
Ryan T. Vest ◽  
Liana N. Bonanno ◽  
Benoit Lehallier ◽  
...  

Author(s):  
Lai Wei ◽  
Siqi Ming ◽  
Bin Zou ◽  
Yongjian Wu ◽  
Zhongsi Hong ◽  
...  

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Elena N. Judd ◽  
Alison R. Gilchrist ◽  
Nicholas R. Meyerson ◽  
Sara L. Sawyer

Abstract Background The Type I interferon response is an important first-line defense against viruses. In turn, viruses antagonize (i.e., degrade, mis-localize, etc.) many proteins in interferon pathways. Thus, hosts and viruses are locked in an evolutionary arms race for dominance of the Type I interferon pathway. As a result, many genes in interferon pathways have experienced positive natural selection in favor of new allelic forms that can better recognize viruses or escape viral antagonists. Here, we performed a holistic analysis of selective pressures acting on genes in the Type I interferon family. We initially hypothesized that the genes responsible for inducing the production of interferon would be antagonized more heavily by viruses than genes that are turned on as a result of interferon. Our logic was that viruses would have greater effect if they worked upstream of the production of interferon molecules because, once interferon is produced, hundreds of interferon-stimulated proteins would activate and the virus would need to counteract them one-by-one. Results We curated multiple sequence alignments of primate orthologs for 131 genes active in interferon production and signaling (herein, “induction” genes), 100 interferon-stimulated genes, and 100 randomly chosen genes. We analyzed each multiple sequence alignment for the signatures of recurrent positive selection. Counter to our hypothesis, we found the interferon-stimulated genes, and not interferon induction genes, are evolving significantly more rapidly than a random set of genes. Interferon induction genes evolve in a way that is indistinguishable from a matched set of random genes (22% and 18% of genes bear signatures of positive selection, respectively). In contrast, interferon-stimulated genes evolve differently, with 33% of genes evolving under positive selection and containing a significantly higher fraction of codons that have experienced selection for recurrent replacement of the encoded amino acid. Conclusion Viruses may antagonize individual products of the interferon response more often than trying to neutralize the system altogether.


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