Pir-B inhibits the DC function and disturbs the Th17/Treg balance in lung cancer murine model
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Huaxing Wu1, Xiaoyu Zheng1, Linlin Dong1, Chunfeng Li1, Mingyue Zhang1, Guonian Wang1,* and Kun Wang1,*
1Department of Anesthesiology, Harbin Medical University Cancer Hospital, Harbin 150081, China
*These authors have contributed equally to this work
Kun Wang, email: email@example.com
Guonian Wang, email: firstname.lastname@example.org
Keywords: Pir-B; Th17; Treg; immune; lung cancer
Received: April 18, 2017 Accepted: September 18, 2017 Published: October 10, 2017
Paired immunoglobulin-like receptor B (Pir-B) was an inhibitory receptor expressed on the surfaces of dendritic cells (DCs). Pir-B inhibit T helper (Th) 1 response and induce Th2 cell differentiation, leading to the imbalance of Th1/Th2 cells. However, the role and potential mechanism of Pir-B on the balance of Th17/regulatory T cells (Tregs) is still largely unknown in lung cancer murine model. In the present study, the DC function and Th17/Treg balance were destroyed during the progression of lung cancer and this was accompanied by an increased expression of Pir-B. After transfection with Pir-B siRNA or administration of IL-6 in vitro, the decreased response of Th17 cells were restored, whereas the augmented differentiation of Tregs was diminished. Further, the transfer of Pir-B silenced DCs or the injection of IL-6 in vivo increased Th17 response and decreased Treg differentiation. Our study has demonstrated that Pir-B inhibits the DC function and disturbs the Th17/Treg balance via IL-6 pathway during the progression of lung cancer, contributing to inhibited antitumor immunity.
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