Year: 2025
Type: article
Abstract: ABSTRACT Abatacept is a CTLA4‐Ig fusion protein that blocks CD80/CD86‐dependent T‐cell co‐stimulation. When administered, Abatacept limits, to a variable degree, loss of stimulated C‐peptide secretion in patients with newly‐diagnosed type 1 diabetes (T1D), while reducing both circulating memory CD4 + T‐cells and T follicular helper (Tfh) cells; however, its precise mechanism of action is not known. To investigate this effect, we studied 12 patients, using multi‐parameter flow cytometry, who each self‐administered Abatacept in subcutaneous formulation for 6 months within 100 days of diagnosis. Abatacept treatment impacted the CD4 + T cell memory compartment, inducing a reduction in T‐effector cells across both conventional (Tconv) and regulatory (Treg) sub‐populations. A reduction in activated Tfh cells (CXCR5 + PD1 + ICOS + ), previously described with intravenous therapy, was replicated and extended. An integrated baseline immunological phenotype predicted Abatacept‐induced preservation of C‐peptide.
DOI: 10.1002/dmrr.70074
Institutions: University of London, Queen Mary University of London, Cambridge University Hospitals NHS Foundation Trust, Addenbrooke's Hospital, Blizard Institute, King's College London, Guy's and St Thomas' NHS Foundation Trust, National Institute for Health and Care Research, Guy's Hospital, Kings Health Partners
Language: English
Subfield: Genetics
Domain: Life Sciences
Open Access status: hybrid
Estimated APC paid: $4,780
OpenAlex ID: W4413106989