Solution structure and synaptic analyses reveal determinants of bispecific T cell engager potency

A Alexander Leithner (The Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Oxford, Roosevelt Drive) O Oskar Staufer (The Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Oxford, Roosevelt Drive) T Tanmay Mitra (The Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Oxford, Roosevelt Drive) F Falk Liberta (Boehringer Ingelheim Pharma GmbH & Co. Kg.) S Salvatore Valvo (The Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Oxford, Roosevelt Drive) M Mikhail Kutuzov (Sir William Dunn School of Pathology, University of Oxford, South Parks Road) H Hannah Dada (The Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Oxford, Roosevelt Drive) J Jacob Spaeth (The Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Oxford, Roosevelt Drive) W Weijie Zhou (Biotherapeutics Discovery, Boehringer Ingelheim) F Felix Schiele (Boehringer Ingelheim Pharma GmbH & Co. Kg.) S Sophia Reindl (Boehringer Ingelheim Pharma GmbH & Co. Kg.) H Herbert Nar (Boehringer Ingelheim Pharma GmbH & Co. Kg.) S Stefan Hoerer (Boehringer Ingelheim Pharma GmbH & Co. Kg.) M Maureen Crames (Biotherapeutics Discovery, Boehringer Ingelheim) S Stephen Comeau (Biotherapeutics Discovery, Boehringer Ingelheim) D David Young (Biotherapeutics Discovery, Boehringer Ingelheim) S Sarah Low (Biotherapeutics Discovery, Boehringer Ingelheim) E Edward Jenkins (The Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Oxford, Roosevelt Drive) S Simon J. Davis (Medical Research Council Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital) D David Klenerman (Department of Chemistry, University of Cambridge) A Andrew Nixon (Biotherapeutics Discovery, Boehringer Ingelheim) N Noah Pefaur (Biotherapeutics Discovery, Boehringer Ingelheim) D David Wyatt (Boehringer Ingelheim Pharma GmbH & Co. Kg.) O Omer Dushek (Sir William Dunn School of Pathology, University of Oxford, South Parks Road) S Srinath Kasturirangan (Biotherapeutics Discovery, Boehringer Ingelheim) M Michael L. Dustin

Abstract

Bispecific T cell engagers (TcEs) link T cell receptors to tumor-associated antigens on cancer cells, forming cytotoxic immunological synapses (IS). Close membrane-to-membrane contact (≤13 nm) has been proposed as a key mechanism of TcE function. To investigate this and identify potential additional mechanisms, we compared four immunoglobulin G1-based (IgG1) TcE Formats (A–D) targeting CD3ε and Her2, designed to create varying intermembrane distances (A < B < C < D). Small-angle X-ray scattering (SAXS) and modeling of the conformational states of isolated TcEs and TcE–antigen complexes predicted close contacts (≤13 nm) for Formats A and B and far contacts (≥18 nm) for Formats C and D. In supported lipid bilayer (SLB) model interfaces, Formats A and B recruited, whereas Formats C and D repelled, CD2–CD58 interactions. Formats A and B also excluded bulky Quantum dots more effectively. SAXS also revealed that TcE–antigen complexes formed by Formats A and C were less flexible than complexes formed by Formats B and D. Functional data with Her2-expressing tumor cells showed cytotoxicity, surface marker expression, and cytokine release following the order A > B = C > D. In a minimal system for IS formation on SLBs, TcE performance followed the trend A = B = C > D. Addition of close contact requiring CD58 costimulation revealed phospholipase C-γ activation matching cytotoxicity with A > B = C > D. Our findings suggest that when adhesion is equivalent, TcE potency is determined by two parameters: contact distance and flexibility. Both the close/far-contact formation axis and the low/high flexibility axis significantly impact TcE potency, explaining the similar potency of Format B (close contact/high flexibility) and C (far contact/low flexibility).

Article Details

Volume / Issue Vol. 122, Issue 22
Published June 03, 2025
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (26)

A

Alexander Leithner

The Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Oxford, Roosevelt Drive

O

Oskar Staufer

The Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Oxford, Roosevelt Drive

T

Tanmay Mitra

The Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Oxford, Roosevelt Drive

F

Falk Liberta

Boehringer Ingelheim Pharma GmbH & Co. Kg.

S

Salvatore Valvo

The Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Oxford, Roosevelt Drive

M

Mikhail Kutuzov

Sir William Dunn School of Pathology, University of Oxford, South Parks Road

H

Hannah Dada

The Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Oxford, Roosevelt Drive

J

Jacob Spaeth

The Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Oxford, Roosevelt Drive

W

Weijie Zhou

Biotherapeutics Discovery, Boehringer Ingelheim

F

Felix Schiele

Boehringer Ingelheim Pharma GmbH & Co. Kg.

S

Sophia Reindl

Boehringer Ingelheim Pharma GmbH & Co. Kg.

H

Herbert Nar

Boehringer Ingelheim Pharma GmbH & Co. Kg.

S

Stefan Hoerer

Boehringer Ingelheim Pharma GmbH & Co. Kg.

M

Maureen Crames

Biotherapeutics Discovery, Boehringer Ingelheim

S

Stephen Comeau

Biotherapeutics Discovery, Boehringer Ingelheim

D

David Young

Biotherapeutics Discovery, Boehringer Ingelheim

S

Sarah Low

Biotherapeutics Discovery, Boehringer Ingelheim

E

Edward Jenkins

The Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Oxford, Roosevelt Drive

S

Simon J. Davis

Medical Research Council Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital

D

David Klenerman

Department of Chemistry, University of Cambridge

A

Andrew Nixon

Biotherapeutics Discovery, Boehringer Ingelheim

N

Noah Pefaur

Biotherapeutics Discovery, Boehringer Ingelheim

D

David Wyatt

Boehringer Ingelheim Pharma GmbH & Co. Kg.

O

Omer Dushek

Sir William Dunn School of Pathology, University of Oxford, South Parks Road

S

Srinath Kasturirangan

Biotherapeutics Discovery, Boehringer Ingelheim

M

Michael L. Dustin