Mouse Anti-BTN3A1 Recombinant Antibody (clone 103.2) (CAT#: PABL-415)

Girard, Pauline, et al. "Potent bidirectional cross-talk between plasmacytoid dendritic cells and γδT cells through BTN3A, type I/II IFNs and immune checkpoints." Frontiers in Immunology 11 (2020): 861.

This study investigates the potent bidirectional cross-talk between plasmacytoid dendritic cells (pDCs) and γδ T cells through BTN3A, type I/II interferons, and immune checkpoints. By co-culturing purified human pDCs and γδ T cells in the presence of various stimulants such as TLR-L, PAg, and zoledronate (Zol), the researchers aimed to mimic both infectious and tumor settings. The study found that TLR7/9L- or Zol-stimulated pDCs drive robust γδ T cell activation, Th1 cytokine secretion, and cytotoxic activity. Conversely, PAg-activated γδ T cells induce phenotypic changes and functional activities in pDCs. The study highlights the crucial interplay between these immune players, suggesting that exploiting this interaction could offer novel immunotherapeutic strategies for cancers, infections, and autoimmune diseases.
Creative Biolabs contributed to this research by providing the anti-BTN3A blocking antibody (Cat# PABL-415). This antibody was pivotal in experiments aimed at blocking BTN3A, a molecule critical in the pDC-γδ T cell cross-talk. The use of this antibody allowed the researchers to delineate the role of BTN3A in the activation and modulation of immune responses between pDCs and γδ T cells, thereby supporting the study's exploration of new therapeutic approaches targeting these interactions.

Farrington, Lila A., et al. "Opsonized antigen activates Vδ2+ T cells via CD16/FCγRIIIa in individuals with chronic malaria exposure." PLoS Pathogens 16.10 (2020): e1008997.

This study investigates the activation and function of Vδ2+ T cells in individuals with chronic malaria exposure. It focuses on how opsonized antigens activate these T cells via the CD16/FCγRIIIa receptor. The researchers demonstrated that in individuals with repeated malaria exposure, Vδ2 T cells show reduced TCR responsiveness but increased expression of CD16. This shift allows Vδ2 T cells to respond to opsonized P. falciparum-infected red blood cells through CD16, independent of TCR engagement. The study highlights a novel activation pathway for Vδ2 T cells that might enhance the immune response against malaria in chronically exposed individuals.
Creative Biolabs provided critical reagents for this research, specifically the Butyrophilin 3A1 (BTN3A1) blocking antibody (Cat# PABL-415). This antibody was essential for experiments demonstrating that Vδ2 T cell activation via CD16 is independent of TCR engagement. By using this antibody, the researchers were able to confirm that BTN3A1 blockade did not inhibit the activation of Vδ2 T cells by opsonized antigens, thereby underscoring the significance of CD16-mediated activation pathways. The contribution of Creative Biolabs' products was crucial in elucidating these alternative activation mechanisms of Vδ2 T cells.

de Weerdt, Iris, et al. "A bispecific single-domain antibody boosts autologous Vγ9Vδ2-T cell responses toward CD1d in chronic lymphocytic leukemia." Clinical Cancer Research 27.6 (2021): 1744-1755.

This study focuses on enhancing the efficacy and reducing the toxicity of autologous T cell-based therapies for chronic lymphocytic leukemia (CLL) by utilizing a bispecific single-domain antibody that targets CD1d to activate Vγ9Vδ2-T cells. The researchers evaluated CD1d expression in 78 untreated CLL patients and generated a CD1d-specific Vγ9Vδ2-T cell engager using single-domain antibodies (VHH). They demonstrated that CD1d is expressed in the majority of CLL patients, particularly those with advanced disease, and that the bispecific engager effectively activates Vγ9Vδ2-T cells, inducing robust cytotoxic responses against CLL cells. The study highlights the potential of this approach to improve the therapeutic outcomes for CLL patients by leveraging the intrinsic immunotherapeutic properties of Vγ9Vδ2-T cells.
Creative Biolabs contributed to this research by providing the anti-BTN3A1 monoclonal antibody (Cat# PABL-415). This antibody was crucial for the experiments that involved blocking BTN3A1 to investigate the remaining phosphoantigen recognition by Vγ9Vδ2-T cells in the presence of the bispecific engager. The use of this antibody allowed the researchers to confirm the additional activation pathway of Vγ9Vδ2-T cells, thus supporting the study's goal of developing more effective and targeted immunotherapies for CLL.

Girard, Pauline, et al. "Dysfunctional BTN3A together with deregulated immune checkpoints and type I/II IFN dictate defective interplay between pDCs and γδ T cells in melanoma patients, which impacts clinical outcomes." Clinical & Translational Immunology 10.11 (2021): e1329.

This study investigates the dysfunctional BTN3A and its interaction with deregulated immune checkpoints and type I/II interferons in the context of melanoma. The research focuses on the roles of plasmacytoid dendritic cells (pDCs) and gamma-delta (γδ) T cells, examining their phenotypic and functional interactions in both the blood and tumor microenvironment of melanoma patients. The study highlights severe alterations in the bidirectional cross-talk between pDCs and γδ T cells in melanoma, noting that while healthy pDCs can drive potent activation of γδ T cells, those from melanoma patients exhibit impaired functionality.
Creative Biolabs provided critical reagents for this study, specifically anti-BTN3A agonist antibody (clone 20.1, Cat# PABL-414) and anti-BTN3A blocking antibody (clone 103.2, Cat# PABL-415). These antibodies were used to assess the functionality of BTN3A on γδ T cells and pDCs within PBMCs and tumor infiltrates. The use of these antibodies was essential in revealing the potential functional impairment of BTN3A in melanoma patients, thereby providing insights into the therapeutic targeting of BTN3A to improve immune responses in cancer therapy​.