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

Ning, Yongling ; Xu, Dongqin ; Zhang, Xiaohang ; Bai, Yu ; Ding, Jun ; Feng, Tongbao ; Wang, Shizhong ; Xu, Ning LU ; Qian, Keqing and Wang, Yong , et al. (2016) In International Journal of Cancer 138(11). p.2713-2723
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... (More)
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. This article is protected by copyright. All rights reserved. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
International Journal of Cancer
volume
138
issue
11
pages
2713 - 2723
publisher
John Wiley & Sons Inc.
external identifiers
  • pmid:26773960
  • scopus:84958554574
  • wos:000372913400017
  • pmid:26773960
ISSN
0020-7136
DOI
10.1002/ijc.30002
language
English
LU publication?
yes
id
fa68856a-1c2e-47a6-be69-3daae23ec47f (old id 8577526)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/26773960?dopt=Abstract
date added to LUP
2016-04-04 07:07:36
date last changed
2022-02-20 19:57:56
@article{fa68856a-1c2e-47a6-be69-3daae23ec47f,
  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. This article is protected by copyright. All rights reserved.}},
  author       = {{Ning, Yongling and Xu, Dongqin and Zhang, Xiaohang and Bai, Yu and Ding, Jun and Feng, Tongbao and Wang, Shizhong and Xu, Ning and Qian, Keqing and Wang, Yong and Qi, Chunjian}},
  issn         = {{0020-7136}},
  language     = {{eng}},
  month        = {{01}},
  number       = {{11}},
  pages        = {{2713--2723}},
  publisher    = {{John Wiley & Sons Inc.}},
  series       = {{International Journal of Cancer}},
  title        = {{β-Glucan restores tumor-educated dendritic cell maturation to enhance antitumor immune responses.}},
  url          = {{http://dx.doi.org/10.1002/ijc.30002}},
  doi          = {{10.1002/ijc.30002}},
  volume       = {{138}},
  year         = {{2016}},
}