ArticleJournal of cellular and molecular medicine2026
Pretreatment With BTK Inhibitors Improved the Sensitivity of DLBCL Cells to CAR-T Cells in a Coculture System by Downregulating the Polarisation of M2 Macrophages.
Article in Journal of cellular and molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Pretreatment With BTK Inhibitors Improved the Sensitivity of DLBCL Cells to CAR-T Cells in a Coculture System by Downregulating the Polarisation of M2 Macrophages.Journal of cellular and molecular medicine · 2026Article
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7 authors.
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Abstract
The tumour microenvironment (TME) of relapsed/refractory (R/R) diffuse large B-cell lymphoma (DLBCL) patients is associated with resistance of DLBCL cells to CD19 CAR-T cells. How to improve TME in DLBCL and improve the efficacy of CAR-T cell therapy remains to be further explored. We observed the sensitivity of HBL-1/U2932 cells pretreated with BTK inhibitors (BTKi) to CAR-T cells with flow cytometry (FCM). The effect of pretreatment of BTKi on the polarisation state of alternative activated M2 macrophages was observed with FCM, real-time PCR and Western blot method. The effect of Notch1 agonist on expressions of Arg-1 protein, iNOS protein, Notch1 protein and RBP-J protein in alternative activated M2 macrophages was observed by Western blot method. Then the expression consistency of Notch-1 and RBP-J in activated M2 macrophages was observed by siRNA transfection of Notch-1. The cytotoxicity of CD19 CAR-T cells on HBL-1/U2932 cells pretreated with ibrutinib/orelabrutinib was higher than that of HBL-1/U2932 cells unpretreated with ibrutinib/orelabrutinib. Cytotoxicity of CAR-T cells to HBL-1 cells in coculture system with alternative activated M2 macrophages was very low. This drug resistance could be reversed by replacing the M2 macrophages (M2 macrophages after 48 h pretreatment with BTKi) in coculture system. Pretreatment with BTKi could down-regulate the expression of CD206 and IL-10 in activated M2 macrophages. And pretreatment with BTKi down-regulated the expression of Arg-1 and upregulated the expression of iNOS in activated M2 macrophages. The upregulation polarisation of M2 macrophages by Notch1 agonist could be reversed by BTKi. Expression of RBP-J protein decreased in alternative activated M2 macrophages by siRNA silencing Notch 1. Pretreatment with BTKi could down-regulate the polarisation of M2 macrophages and reverse the resistance of DLBCL cells which were cocultured with alternative activated M2 macrophages to CAR-T cells. This effect might be achieved by downregulating the Notch-RBP-J pathway.
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