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Calcipotriol, a synthetic Vitamin D analog, promotes antitumor immunity via CD4+T-dependent CTL/NK cell activationopen access

Authors
Kim, H.Kim, J.Sa, J.K.Ryu, B.-K.Park, K.-J.Kim, J.Ha, H.Park, Y.Shin, M.H.Kim, J.Lee, H.Kim, D.Lee, K.Jang, B.Lee, K.-M.Kang, S.-H.
Issue Date
10월-2022
Publisher
Elsevier Masson s.r.l.
Keywords
Antitumor immunity; Calcipotriol; Glioblastoma; TSLP/CD4+T cell axis
Citation
Biomedicine and Pharmacotherapy, v.154
Indexed
SCIE
SCOPUS
Journal Title
Biomedicine and Pharmacotherapy
Volume
154
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/144145
DOI
10.1016/j.biopha.2022.113553
ISSN
0753-3322
Abstract
To overcome the hurdles of immunotherapy, we investigated whether calcipotriol, a synthetic vitamin D analog, could overcome the immune evasion of glioblastoma multiforme (GBM) by modulating immune responses and the immunosuppressive tumor microenvironment. Administration of calcipotriol considerably reduced tumor growth. Both in vivo and in vitro studies revealed that CD8+T and natural killer (NK) cell gene signatures were enriched and activated, producing high levels of IFN-γ and granzyme B. In contrast, regulatory T cells (Treg) were significantly reduced in the calcipotriol-treated group. The expression of CD127, the receptor for thymic stromal lymphopoietin (TSLP), is elevated in CD4+T cells and potentially supports T-cell priming. Depleting CD4+T cells, but not NK or CD8+T cells, completely abrogated the antitumor efficacy of calcipotriol. These data highlight that the calcipotriol/TSLP/CD4+T axis can activate CD8+T and NK cells with a concomitant reduction in the number of Tregs in GBM. Therefore, calcipotriol can be a novel therapeutic modality to overcome the immune resistance of GBM by converting immunologically “cold” tumors into “hot” tumors. Data availability: Data are available upon reasonable request. The RNA-seq dataset comparing the transcriptomes of control and calcipotriol-treated GL261 tumors is available from the corresponding author upon request. © 2022 The Authors
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