Ibrutinib for improved chimeric antigen receptor T-cell production for chronic lymphocytic leukemia patients.


Journal

International journal of cancer
ISSN: 1097-0215
Titre abrégé: Int J Cancer
Pays: United States
ID NLM: 0042124

Informations de publication

Date de publication:
15 01 2021
Historique:
received: 04 03 2020
revised: 05 06 2020
accepted: 03 07 2020
pubmed: 20 7 2020
medline: 9 6 2021
entrez: 20 7 2020
Statut: ppublish

Résumé

Chimeric antigen receptor T (CART) cells targeting CD19 have shown promising results in the treatment of chronic lymphocytic leukemia (CLL). However, efficacy seems to be inferior compared to diffuse large B-cell lymphoma or acute lymphoblastic leukemia. Impaired T-cell fitness of CLL patients may be involved in treatment failure. Less-differentiated naïve-like T cells play an important role in CART expansion and long-term persistence in vivo. These cells are sparse in CLL patients. Therefore, optimization of CART cell production protocols enriching less differentiated T cell subsets may overcome treatment resistance. The B-cell receptor inhibitor ibrutinib targeting Bruton's tyrosine kinase (BTK) is approved for the treatment of CLL. Besides BTK, ibrutinib additionally inhibits interleukin-2-inducible T-cell kinase (ITK) which is involved in T-cell differentiation. To evaluate the effect of ibrutinib on CART cell production, peripheral blood mononuclear cells from nine healthy donors and eight CLL patients were used to generate CART cells. T-cell expansion and phenotype, expression of homing and exhaustion makers as well as functionality of CART cells were evaluated. CART cell generation in the presence of ibrutinib resulted in increased cell viability and expansion of CLL patient-derived CART cells. Furthermore, ibrutinib enriched CART cells with less-differentiated naïve-like phenotype and decreased expression of exhaustion markers including PD-1, TIM-3 and LAG-3. In addition, ibrutinib increased the cytokine release capacity of CLL patient-derived CART cells. In summary, BTK/ITK inhibition with ibrutinib during CART cell culture can improve yield and function of CLL patient-derived CART cell products.

Identifiants

pubmed: 32683672
doi: 10.1002/ijc.33212
doi:

Substances chimiques

Antigens, CD19 0
CD19 molecule, human 0
CD19-specific chimeric antigen receptor 0
Culture Media 0
Cytokines 0
Piperidines 0
Receptors, Antigen, T-Cell 0
Receptors, Chimeric Antigen 0
ibrutinib 1X70OSD4VX
Adenine JAC85A2161

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

419-428

Informations de copyright

© 2020 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of Union for International Cancer Control.

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Auteurs

Fuli Fan (F)

Department of Internal Medicine V, Heidelberg University Hospital, Heidelberg, Germany.

Hyeon Joo Yoo (HJ)

Department of Internal Medicine V, Heidelberg University Hospital, Heidelberg, Germany.

Sophia Stock (S)

Department of Internal Medicine V, Heidelberg University Hospital, Heidelberg, Germany.

Lei Wang (L)

Department of Internal Medicine V, Heidelberg University Hospital, Heidelberg, Germany.

Yibin Liu (Y)

Department of Internal Medicine V, Heidelberg University Hospital, Heidelberg, Germany.

Maria-Luisa Schubert (ML)

Department of Internal Medicine V, Heidelberg University Hospital, Heidelberg, Germany.

Sanmei Wang (S)

Department of Internal Medicine V, Heidelberg University Hospital, Heidelberg, Germany.

Brigitte Neuber (B)

Department of Internal Medicine V, Heidelberg University Hospital, Heidelberg, Germany.

Angela Hückelhoven-Krauss (A)

Department of Internal Medicine V, Heidelberg University Hospital, Heidelberg, Germany.

Ulrike Gern (U)

Department of Internal Medicine V, Heidelberg University Hospital, Heidelberg, Germany.

Anita Schmitt (A)

Department of Internal Medicine V, Heidelberg University Hospital, Heidelberg, Germany.

Carsten Müller-Tidow (C)

Department of Internal Medicine V, Heidelberg University Hospital, Heidelberg, Germany.
National Center for Tumor Diseases (NCT), German Cancer Consortium (DKTK), Heidelberg, Germany.

Peter Dreger (P)

Department of Internal Medicine V, Heidelberg University Hospital, Heidelberg, Germany.
National Center for Tumor Diseases (NCT), German Cancer Consortium (DKTK), Heidelberg, Germany.

Michael Schmitt (M)

Department of Internal Medicine V, Heidelberg University Hospital, Heidelberg, Germany.
National Center for Tumor Diseases (NCT), German Cancer Consortium (DKTK), Heidelberg, Germany.

Leopold Sellner (L)

Department of Internal Medicine V, Heidelberg University Hospital, Heidelberg, Germany.
National Center for Tumor Diseases (NCT), German Cancer Consortium (DKTK), Heidelberg, Germany.
Oncology Business Unit - Medical Affairs, Takeda Pharma Vertrieb GmbH & Co. KG, Berlin, Germany.

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