Influence of Galectin-9/Tim-3 Interaction on Herpes Simplex Virus-1 Latency
作者： Pradeep B. J. Reddy , Sharvan Sehrawat , Amol Suryawanshi , Naveen K. Rajasagi , Sachin Mulik
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摘要: After HSV-1 infection, CD8(+) T cells accumulate in the trigeminal ganglion (TG) and participate maintenance of latency. However, mechanisms underlying intermittent virus reactivation are poorly understood. In this study, we demonstrate role an inhibitory interaction between cell Ig mucin domain-containing molecule 3 (Tim-3)-expressing galectin 9 (Gal-9) that could influence latency reactivation. Accordingly, show most K(b)-gB tetramer-specific TG HSV-1-infected mice express Tim-3, a delivers negative signals to upon engagement its ligand Gal-9. Gal-9 was also upregulated when replicating present as well during This set stage for Gal-9/Tim-3 interaction, responsible reduced effector function wild-type mice. Additionally, cultures exposed recombinant latent phase caused apoptosis cells. Furthermore, knockout showed delayed viral compared with cultures, demonstrating greater efficiency inhibit absence Moreover, addition ex vivo induced enhanced untreated controls. Our results host homeostatic mechanism mediated by on can outcome manipulating might represent therapeutic means from
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