CD1d expression in glioblastoma is a promising target for NKT cell-based cancer immunotherapy.


Journal

Cancer immunology, immunotherapy : CII
ISSN: 1432-0851
Titre abrégé: Cancer Immunol Immunother
Pays: Germany
ID NLM: 8605732

Informations de publication

Date de publication:
May 2021
Historique:
received: 09 05 2020
accepted: 12 10 2020
pubmed: 1 11 2020
medline: 5 5 2021
entrez: 31 10 2020
Statut: ppublish

Résumé

Glioblastoma is the most common and aggressive type of brain tumor with high recurrence and fatality rates. Although various therapeutic strategies have been explored, there is currently no effective treatment for glioblastoma. Recently, the number of immunotherapeutic strategies has been tested for malignant brain tumors. Invariant natural killer T (iNKT) cells play an important role in anti-tumor immunity. To address if iNKT cells can target glioblastoma to exert anti-tumor activity, we assessed the expression of CD1d, an antigen-presenting molecule for iNKT cells, on glioblastoma cells. Glioblastoma cells from 10 of 15 patients expressed CD1d, and CD1d-positive glioblastoma cells pulsed with glycolipid ligand induced iNKT cell-mediated cytotoxicity in vitro. Although CD1d expression was low on glioblastoma stem-like cells, retinoic acid, which is the most common differentiating agent, upregulated CD1d expression in these cells and induced iNKT cell-mediated cytotoxicity. Moreover, intracranial administration of human iNKT cells induced tumor regression of CD1d-positive glioblastoma in orthotopic xenografts in NOD/Shi-scid IL-2RγKO (NOG) mice. Thus, CD1d expression represents a novel target for NKT cell-based immunotherapy for glioblastoma patients.

Identifiants

pubmed: 33128583
doi: 10.1007/s00262-020-02742-1
pii: 10.1007/s00262-020-02742-1
pmc: PMC8053161
doi:

Substances chimiques

Antigens, CD1d 0
Cancer Vaccines 0
Tretinoin 5688UTC01R

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1239-1254

Subventions

Organisme : Japan Society for the Promotion of Science
ID : #18H0289
Organisme : Japan Society for the Promotion of Science
ID : #17K16625
Organisme : Japan Society for the Promotion of Science
ID : #19K18379

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Auteurs

Ayaka Hara (A)

Department of Medical Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.
Department of Neurological Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.

Ryo Koyama-Nasu (R)

Department of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.

Mariko Takami (M)

Department of Medical Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.

Takahide Toyoda (T)

Department of Medical Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.

Takahiro Aoki (T)

Department of Medical Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.

Fumie Ihara (F)

Department of Medical Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.

Masayoshi Kobayashi (M)

Department of Neurological Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.

Seiichiro Hirono (S)

Department of Neurological Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.

Tomoo Matsutani (T)

Department of Neurological Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.

Toshinori Nakayama (T)

Department of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.

Yasuo Iwadate (Y)

Department of Neurological Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.

Shinichiro Motohashi (S)

Department of Medical Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan. motohashi@faculty.chiba-u.jp.

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