Sign in
Cell BiologybioRxiv
Preprint

Alpha-1 Antitrypsin Overexpressing Mesenchymal Stem/Stromal Cells Reverses Type 1 Diabetes via Promoting Treg Function and CD8+ T cell exhaustion

Hua WeiiD, Wenyu GouiD, Judong KimiD, Suganya SubramanianiD, Tiffany Yeung, Paramita ChakrabortyiD, Shikhar MehrotraiD, Stefano BertoiD, Charlie StrangeiD, Hongjun WangiD

Abstract

Mesenchymal stem/stromal cell (MSC) therapy holds great promise as both a therapeutic option and as a biofactory, as cells produce therapeutic proteins to augment their efficacy in disease treatment. This study investigates the therapeutic effects and the mechanistic insights of alpha-1 antitrypsin overexpressing MSCs (AAT-MSCs) in diabetes prevention and treatment. A single infusion of AAT-MSCs not only delayed diabetes onset but reversed new-onset type 1 diabetes (T1D) in the nonobese diabetic (NOD) mice. Using single-cell RNA sequencing, flow cytometry, and functional analyses, we characterized the impact of AAT-MSCs on immune cells, particularly CD4+ and CD8+ T cells, in pancreatic lymph nodes (PLNs) and islets of NOD mice. AAT-MSCs enhanced the immunosuppressive function and the communication of regulatory T cells (Tregs) with other immune cells while reducing the numbers of T helper 1 (Th1) cells and CD8+ cytotoxic T cells. In vitro experiments further confirmed the capacity of AAT-MSCs to promote the proliferation of Tregs, which consequently fostered an exhausted phenotype in CD8+ T cells, thereby facilitating {beta} cell survival and potentially aiding in diabetes remission. Thus, our findings underscore the significant protective effects of AAT-MSCs, delineate their novel mechanistic insight on recipient immune cells, and provide evidence for the clinical application of AAT-MSCs in treating T1D.

PDFDOI

02 /Specification & Classification

Click any tag to browse matching papers

Reproducibility ledger

Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.

Sign in to file a reproducibility report.