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Hence, immunomodulation of pancreas\u2010infiltrated immune cells especially the <jats:italic>\u03b2<\/jats:italic>\u2010cells autoreactive\u2010T cells is a promising way to hinder and reverse the progress of T1D. Herein, megakaryocytes are primed with interferon\u2010<jats:italic>\u03b3<\/jats:italic> (IFN\u2010<jats:italic>\u03b3<\/jats:italic>) to produce platelets presenting high levels of immunosuppressive checkpoint ligands including programmed death\u2010ligand 1 (PD\u2010L1), Programmed Death\u2010Ligand 2 (PD\u2010L2), the B and T lymphocyte attenuator (BTLA) and Galectin\u20109 (Gal\u20109), termed as IFN\u2010<jats:italic>\u03b3<\/jats:italic> platelets. The IFN\u2010<jats:italic>\u03b3<\/jats:italic> platelets bound and interacted with T cells through immune checkpoint ligands and receptors, which efficaciously induced T cell exhaustion and apoptosis in vitro. Virtually, NOD diabetes mice received IFN\u2010<jats:italic>\u03b3<\/jats:italic> platelets treatments prominently preserved <jats:italic>\u03b2<\/jats:italic>\u2010cell integrity and insulin production, ultimately hindering the progress to hyperglycemia. Intriguingly, both the amount and activity of the pancreas infiltrate\u2010T cells intensively reduced, whereas the magnitude of regulatory T cells (Tregs) remarkably increased, which is attributed to IFN\u2010<jats:italic>\u03b3<\/jats:italic> platelets treatments. Moreover, IFN\u2010<jats:italic>\u03b3<\/jats:italic> platelets treatment instigated macrophage polarization toward an anti\u2010inflammatory M2 phenotype that may stimulate pancreatic angiogenesis, and promote <jats:italic>\u03b2<\/jats:italic>\u2010cell proliferation, consequently ameliorating the new\u2010onset T1D.<\/jats:p>","DOI":"10.1002\/advs.202501139","type":"journal-article","created":{"date-parts":[[2025,3,4]],"date-time":"2025-03-04T05:58:46Z","timestamp":1741067926000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Bioengineering Platelets Presenting PD\u2010L1, Galectin\u20109 and BTLA to Ameliorate Type 1 Diabetes"],"prefix":"10.1002","volume":"12","author":[{"given":"Yumeng","family":"Ma","sequence":"first","affiliation":[{"name":"Shenzhen Key Laboratory for Systems Medicine in Inflammatory Diseases School of Medicine Shenzhen Campus of Sun Yat\u2010Sen University Sun Yat\u2010Sen University  Shenzhen Guangdong 518107 P. 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