TGF-β inhibition via CRISPR promotes the long-term efficacy of CAR T cells against solid tumors

In recent years, chimeric antigen receptor-modified T cell (CAR T cell) therapy has proven to be a promising approach against cancer. Nonetheless, this approach still faces multiple challenges in eliminating solid tumors, one of which being the immunosuppressive tumor microenvironment (TME). Here, w...

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Published in:JCI insight Vol. 5; no. 4
Main Authors: Tang, Na, Cheng, Chen, Zhang, Xingying, Qiao, Miaomiao, Li, Na, Mu, Wei, Wei, Xiao-Fei, Han, Weidong, Wang, Haoyi
Format: Journal Article
Language:English
Published: United States American Society for Clinical Investigation 27.02.2020
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ISSN:2379-3708, 2379-3708
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Abstract In recent years, chimeric antigen receptor-modified T cell (CAR T cell) therapy has proven to be a promising approach against cancer. Nonetheless, this approach still faces multiple challenges in eliminating solid tumors, one of which being the immunosuppressive tumor microenvironment (TME). Here, we demonstrated that knocking out the endogenous TGF-β receptor II (TGFBR2) in CAR T cells with CRISPR/Cas9 technology could reduce the induced Treg conversion and prevent the exhaustion of CAR T ce lls. Meanwhile, TGFBR2-edited CAR T cells had better in vivo tumor elimination efficacy, both in cell line-derived xenograft and patient-derived xenograft solid tumor models, whether administered locally or systemically. In addition, the TGFBR2-edited CAR T cells could eliminate contralaterally reinoculated xenografts in mice effectively, with an increased proportion of memory subsets within circulating CAR T cells of central memory and effector memory subsets. In conclusion, we greatly improved the in vitro and in vivo function of CAR T cells in TGF-β-rich tumor environments by knocking out endogenous TGFBR2 and propose a potentially new method to improve the efficacy of CAR T cell therapy for treating solid tumors.
AbstractList In recent years, chimeric antigen receptor-modified T cell (CAR T cell) therapy has proven to be a promising approach against cancer. Nonetheless, this approach still faces multiple challenges in eliminating solid tumors, one of which being the immunosuppressive tumor microenvironment (TME). Here, we demonstrated that knocking out the endogenous TGF-β receptor II (TGFBR2) in CAR T cells with CRISPR/Cas9 technology could reduce the induced Treg conversion and prevent the exhaustion of CAR T ce lls. Meanwhile, TGFBR2-edited CAR T cells had better in vivo tumor elimination efficacy, both in cell line-derived xenograft and patient-derived xenograft solid tumor models, whether administered locally or systemically. In addition, the TGFBR2-edited CAR T cells could eliminate contralaterally reinoculated xenografts in mice effectively, with an increased proportion of memory subsets within circulating CAR T cells of central memory and effector memory subsets. In conclusion, we greatly improved the in vitro and in vivo function of CAR T cells in TGF-β-rich tumor environments by knocking out endogenous TGFBR2 and propose a potentially new method to improve the efficacy of CAR T cell therapy for treating solid tumors.
In recent years, chimeric antigen receptor-modified T cell (CAR T cell) therapy has proven to be a promising approach against cancer. Nonetheless, this approach still faces multiple challenges in eliminating solid tumors, one of which being the immunosuppressive tumor microenvironment (TME). Here, we demonstrated that knocking out the endogenous TGF-β receptor II (TGFBR2) in CAR T cells with CRISPR/Cas9 technology could reduce the induced Treg conversion and prevent the exhaustion of CAR T ce lls. Meanwhile, TGFBR2-edited CAR T cells had better in vivo tumor elimination efficacy, both in cell line-derived xenograft and patient-derived xenograft solid tumor models, whether administered locally or systemically. In addition, the TGFBR2-edited CAR T cells could eliminate contralaterally reinoculated xenografts in mice effectively, with an increased proportion of memory subsets within circulating CAR T cells of central memory and effector memory subsets. In conclusion, we greatly improved the in vitro and in vivo function of CAR T cells in TGF-β-rich tumor environments by knocking out endogenous TGFBR2 and propose a potentially new method to improve the efficacy of CAR T cell therapy for treating solid tumors.In recent years, chimeric antigen receptor-modified T cell (CAR T cell) therapy has proven to be a promising approach against cancer. Nonetheless, this approach still faces multiple challenges in eliminating solid tumors, one of which being the immunosuppressive tumor microenvironment (TME). Here, we demonstrated that knocking out the endogenous TGF-β receptor II (TGFBR2) in CAR T cells with CRISPR/Cas9 technology could reduce the induced Treg conversion and prevent the exhaustion of CAR T ce lls. Meanwhile, TGFBR2-edited CAR T cells had better in vivo tumor elimination efficacy, both in cell line-derived xenograft and patient-derived xenograft solid tumor models, whether administered locally or systemically. In addition, the TGFBR2-edited CAR T cells could eliminate contralaterally reinoculated xenografts in mice effectively, with an increased proportion of memory subsets within circulating CAR T cells of central memory and effector memory subsets. In conclusion, we greatly improved the in vitro and in vivo function of CAR T cells in TGF-β-rich tumor environments by knocking out endogenous TGFBR2 and propose a potentially new method to improve the efficacy of CAR T cell therapy for treating solid tumors.
In recent years, chimeric antigen receptor–modified T cell (CAR T cell) therapy has proven to be a promising approach against cancer. Nonetheless, this approach still faces multiple challenges in eliminating solid tumors, one of which being the immunosuppressive tumor microenvironment (TME). Here, we demonstrated that knocking out the endogenous TGF-β receptor II (TGFBR2) in CAR T cells with CRISPR/Cas9 technology could reduce the induced Treg conversion and prevent the exhaustion of CAR T ce lls. Meanwhile, TGFBR2-edited CAR T cells had better in vivo tumor elimination efficacy, both in cell line–derived xenograft and patient-derived xenograft solid tumor models, whether administered locally or systemically. In addition, the TGFBR2-edited CAR T cells could eliminate contralaterally reinoculated xenografts in mice effectively, with an increased proportion of memory subsets within circulating CAR T cells of central memory and effector memory subsets. In conclusion, we greatly improved the in vitro and in vivo function of CAR T cells in TGF-β–rich tumor environments by knocking out endogenous TGFBR2 and propose a potentially new method to improve the efficacy of CAR T cell therapy for treating solid tumors. Inhibition of the immunosuppressive TGFβ signaling by knocking out endogenous TGFBR2 greatly improved the persistence and efficacy of CAR-T cells against solid tumors in mice.
Author Cheng, Chen
Wang, Haoyi
Qiao, Miaomiao
Zhang, Xingying
Han, Weidong
Li, Na
Tang, Na
Mu, Wei
Wei, Xiao-Fei
AuthorAffiliation 4 Beijing Cord Blood Bank, Beijing, China
6 Department of Molecular Biology and Immunology, Chinese People’s Liberation Army General Hospital, Beijing, China
5 Biotherapeutic Department and
1 State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China
3 University of Chinese Academy of Sciences, Beijing, China
2 School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, China
7 Institute for Stem Cell and Regeneration, Chinese Academy of Sciences, Beijing, China
AuthorAffiliation_xml – name: 6 Department of Molecular Biology and Immunology, Chinese People’s Liberation Army General Hospital, Beijing, China
– name: 4 Beijing Cord Blood Bank, Beijing, China
– name: 2 School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, China
– name: 5 Biotherapeutic Department and
– name: 7 Institute for Stem Cell and Regeneration, Chinese Academy of Sciences, Beijing, China
– name: 1 State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China
– name: 3 University of Chinese Academy of Sciences, Beijing, China
Author_xml – sequence: 1
  givenname: Na
  surname: Tang
  fullname: Tang, Na
– sequence: 2
  givenname: Chen
  surname: Cheng
  fullname: Cheng, Chen
– sequence: 3
  givenname: Xingying
  surname: Zhang
  fullname: Zhang, Xingying
– sequence: 4
  givenname: Miaomiao
  surname: Qiao
  fullname: Qiao, Miaomiao
– sequence: 5
  givenname: Na
  surname: Li
  fullname: Li, Na
– sequence: 6
  givenname: Wei
  surname: Mu
  fullname: Mu, Wei
– sequence: 7
  givenname: Xiao-Fei
  orcidid: 0000-0001-6775-346X
  surname: Wei
  fullname: Wei, Xiao-Fei
– sequence: 8
  givenname: Weidong
  surname: Han
  fullname: Han, Weidong
– sequence: 9
  givenname: Haoyi
  surname: Wang
  fullname: Wang, Haoyi
BackLink https://www.ncbi.nlm.nih.gov/pubmed/31999649$$D View this record in MEDLINE/PubMed
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2020 American Society for Clinical Investigation 2020 American Society for Clinical Investigation
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Snippet In recent years, chimeric antigen receptor-modified T cell (CAR T cell) therapy has proven to be a promising approach against cancer. Nonetheless, this...
In recent years, chimeric antigen receptor–modified T cell (CAR T cell) therapy has proven to be a promising approach against cancer. Nonetheless, this...
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SubjectTerms Antigens
Cancer
Cell therapy
Chimeric antigen receptors
CRISPR
Cytokines
Cytotoxicity
Genes
Immunological memory
Ligands
Lymphocytes
Lymphocytes T
Memory cells
Solid tumors
Transforming growth factor-b
Tumor microenvironment
Tumors
Xenografts
Title TGF-β inhibition via CRISPR promotes the long-term efficacy of CAR T cells against solid tumors
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