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Int J Cancer. 2016 Jun 1;138(11):2713-23. doi: 10.1002/ijc.30002. Epub 2016 Feb 8.

β-glucan restores tumor-educated dendritic cell maturation to enhance antitumor immune responses.

Ning Y1,2, Xu D1, Zhang X1, Bai Y1, Ding J1,2, Feng T1,3, Wang S1, Xu N4, Qian K2, Wang Y3, Qi C1,2.

Author information

1
Medical Research Center, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, 213003, China.
2
Department of Oncology, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, 213003, China.
3
Department of General Surgery, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, 213003, China.
4
Section of Clinical Chemistry & Pharmacology, Department of Laboratory Medicine, Lund University, Lund, S-221 85, Sweden.

Abstract

Tumors can induce the generation and accumulation of immunosuppressive cells such as myeloid-derived suppressor cells (MDSCs) in a tumor microenvironment, contributing to tumor escape from immunological attack. Although dendritic cell-based cancer vaccines can initiate antitumor immune responses, tumor-educated dendritic cells (TEDCs) involved in the tolerance induction have attracted much attention recently. In this study, we investigated the effect of β-glucan on TEDCs and found that β-glucan treatment could promote the maturation and migration of TEDCs and that the suppressive function of TEDCs was significantly decreased. Treatment with β-glucan drastically decreased the levels of regulatory T (Treg) cells but increased the infiltration of macrophages, granulocytes and DCs in tumor masses, thus elicited Th1 differentiation and cytotoxic T-lymphocyte responses and led to a delay in tumor progression. These findings reveal that β-glucan can inhibit the regulatory function of TEDCs, therefore revealing a novel function for β-glucan in immunotherapy and suggesting its potential clinical benefit. β-Glucan directly abrogated tumor-educated dendritic cells-associated immune suppression, promoted Th1 differentiation and cytotoxic T-lymphocyte priming and improved antitumor responses.

KEYWORDS:

T cell differentiation; dendritic cell; immune suppression; tumor immunotherapy; β-Glucan

PMID:
26773960
DOI:
10.1002/ijc.30002
[Indexed for MEDLINE]
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