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. 2011 May 26;6(5):e19664. doi: 10.1371/journal.pone.0019664

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This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

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We have previously shown that HCV core/gC1qR interaction up-regulates PD-1 and SOCS-1 negative signaling molecules, leading to suppression of TLR-mediated IL-12 production. In this study, we further demonstrated that the Tim-3 inhibitory pathway is involved in the HCV core/gC1qR-induced inhibition of IL-12 expression by M/M_Ф during HCV infection. Specifically, we found that Tim-3 can be up-regulated by HCV core/gC1qR interaction, which in turn, inhibits TLR-mediated IL-12 production. We also found that Tim-3 can crosstalk with other inhibitory molecules such as PD-1 and SOCS-1 to coordinately inhibit TLR-mediated IL-12 signaling pathways during HCV infection. We conclude that HCV-mediated innate immune dysregulation (impaired M/M_Ф IL-12 production) may ultimately lead to adaptive Th1/Tc1 dysfunction, and thus, HCV persistence.