Poster Presentation Melbourne Immunotherapy Spring Symposium 2025

Enhancing CAR T-cell Function Via Dual-targeting of 4-1BB and TGF-β (#108)

Arthur (Xuan) Wang 1 2 , Xiao Jing Ong 1 2 , Vicky Qin 1 2 , Criselle DSouza 1 2 , Joe Zhu 1 2 , Paul Neeson 1 2
  1. Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia
  2. The Sir Peter MacCallum Department of Oncology, Faculty of Medicine, Dentistry and Health Science, University of Melbourne, Melbourne, Victoria, Australia

Background: Despite successes in haematological tumours, CAR T-cell therapy remain ineffective in solid tumours owing to the immunosuppressive tumour microenvironment (TME). The lack of T-cell costimulation remain a major challenge within the TME, preventing sufficient T-cell activation and effector function. 4-1BB presents a promising costimulatory molecule to overcome such deficiencies, being associated with CAR T-cell persistence and favourable responses to immune checkpoint blockades. Additionally, the immunosuppressive cytokine TGF-β also suppresses T-cell proliferation and effector functions within the TME, dampening the anti-tumour immune response.

Aims: To enhance CAR T-cell efficacy in solid tumours by targeting both 4-1BB and TGF-β.

Methods: We designed a bi-specific molecule capable of sequestering free TGF-β while activating 4-1BB on T-cells, named Bifunctional Activator Trap (BAT). BAT features a 4-1BB binding domain, IgG Fc region, and a TGF-β binding domain. Purified BAT were produced with the CHO expression system and evaluated both in vitro and in vivo.

Results: BAT reduced high concentrations of free TGF-β to undetectable levels even at low molar ratios in vitro; and completely prevented downstream activations of SMAD signalling in reporter cells. BAT also activated 4-1BB via the NF-κB pathway similar to existing anti-41BB monoclonal antibodies. Such 4-1BB activation were primarily driven by NF-κB rather than AP-1 or MAPK signalling pathways. When co-cultured with activated CAR T-cells, BAT further upregulated the activation markers CD25 and CD69, while simultaneously preventing TGF-β from downregulating CD25 and upregulating PD1. Intraperitoneal administration of BAT in tumour-bearing mice resulted in stable serum drug concentrations, significant BAT distribution in the tumour, and a complete reduction of tumour TGF-β levels. Lastly, systemic administration of BAT enhanced the anti-tumour effect of CAR T-cells without notable toxicities.

Conclusions: BAT effectively prevented TGF-β immunosuppression and provided 4-1BB costimulation in vitro, while showing sufficient stability and efficacy in vivo, allowing for further MoA studies.