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- B cell Maturation Antigen Impacts Microglia and Macrophage Phenotypes in Neuro-autoimmune disease. (Exhibit Hall F1; Poster Board Number: B842) - Mar 29, 2024 - Abstract #IMMUNOLOGY2024IMMUNOLOGY_1430;
In the lymph nodes, we also observed a similar effect on the M1-type macrophages in BCMA-/- mice compared to BCMA+/+ mice. These findings offer evidence of a novel role for BCMA in modulating microglia and macrophage function, providing additional insights into the intricate role that BAFF and APRIL play in neuroautoimmune diseases.
- B cell Maturation Antigen Impacts Microglia and Macrophage Phenotypes in Neuro-autoimmune disease. (Room W181) - Mar 22, 2024 - Abstract #IMMUNOLOGY2024IMMUNOLOGY_320;
In the lymph nodes, we also observed a similar effect on the M1-type macrophages in BCMA-/- mice compared to BCMA+/+ mice. These findings offer evidence of a novel role for BCMA in modulating microglia and macrophage function, providing additional insights into the intricate role that BAFF and APRIL play in neuroautoimmune diseases.
- | Journal, CAR T-Cell Therapy, IO biomarker: Combining BCMA-targeting CAR-T with TCR-engineered T-cell therapy to prevent immune escape of multiple myeloma. (Pubmed Central) - Oct 22, 2023
Furthermore, in an in vivo immune escape model of MM, only a combination of BCMA-CAR-T cells with BOB1-TCR engineered T cells could completely clear tumors from bone marrow of mice bearing heterogenous tumors, whereas single-agent treatment led to progressive outgrowth of immune escaped MM. Collectively, we provide a preclinical rationale of combining HLA-dependent and -independent targeting for the cellular therapy of MM.
- | crenigacestat (LY3039478) / Eli Lilly, BMS
Journal, CAR T-Cell Therapy, IO biomarker: All-trans retinoic acid works synergistically with the γ-secretase inhibitor crenigacestat to augment BCMA on multiple myeloma and the efficacy of BCMA-CAR T cells. (Pubmed Central) - Feb 2, 2023
Taken together, the data show that ATRA treatment leads to enhanced BCMA expression on MM cells and consecutively, enhanced reactivity of BCMA-CAR T cells. The data support the clinical evaluation of ATRA in combination with BCMA-CAR T-cell therapy and potentially, other BCMA-directed immunotherapies.
- | AUTO2 / Autolus
Journal, CAR T-Cell Therapy: Both APRIL and antibody-fragment-based CAR T cells for myeloma induce BCMA downmodulation by trogocytosis and internalization. (Pubmed Central) - Nov 9, 2022
BCMA internalization mostly contributed to this effect, but trogocytosis by CAR T cells was also observed. Our study sheds light on the mechanisms underlying CAR T cell failure in MM when targeting BCMA and can inform the development of improved treatment strategies.
- | crenigacestat (LY3039478) / Eli Lilly, BMS
Journal, CAR T-Cell Therapy, IO biomarker: ATRA works synergistically with the γ-secretase inhibitor crenigacestat to augment BCMA on multiple myeloma and the efficacy of BCMA-CAR T-cells. (Pubmed Central) - Sep 3, 2022
Taken together, the data show that ATRA treatment leads to enhanced BCMA expression on MM cells and consecutively, enhanced reactivity of BCMA-CAR T-cells. The data support the clinical evaluation of ATRA in combination with BCMA-CAR T-cell therapy and potentially, other BCMA-directed immunotherapies.
- ATRA works synergistically with γ-secretase inhibitors to augment BCMA on multiple myeloma and the efficacy of BCMA-CAR T-cells () - Aug 13, 2022 - Abstract #IMW2022IMW_523;
The data support the clinical evaluation of ATRA in combination with BCMA-CAR T-cell therapy and potentially, other BCMA-directed immunotherapies. Taken together, the data show that ATRA treatment augments BCMA expression on MM cell liens and primary MM cells and support the clinical evaluation of ATRA in combination with BCMA-CAR T-cells to augment response rates and duration of response.
- SP600125 / BMS
H3K36 Trimethylation Mediated By SETD2 Regulates Cell Proliferation and Cell Cycle By Modulating BCMA-JNK and c-Myc Pathways in Multiple Myeloma (GWCC - Hall B5, Level 1) - Nov 5, 2021 - Abstract #ASH2021ASH_3816;
Furthermore, blockage of the JNK pathway by its inhibitor SP600125 resulted in significant inhibition of MM cell proliferation induced by SETD2 knockdown...Together, our data delineate that SETD2-dependent H3K36me3 modification plays a critical role in regulation cell proliferation and cell cycle by BCMA-JNK and c-Myc pathways in MM cells. Targeting the SETD2-H3K36me3 pathway represents a promising therapy for MM.
- || PRG1801 / Dr. Reddy's, natural killer cell therapy / Xinxiang Medical University
Review, Journal: The Application of Nanobody in CAR-T Therapy. (Pubmed Central) - Jul 15, 2021
Interestingly, anti-BCMA CAR-T modulated by a single nanobody or bi-valent nanobody displays comparable clinical effects with that of single-chain variable fragment (scFv)-modulated CAR-T. The application of nanobodies in CAR-T therapy has been well demonstrated from bench to bedside and displays great potential in forming advanced CAR-T for more challenging tasks.