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However, adverse events, safety concerns in immunocompromised patients, and disease relapse limit clinical utility. Here, we exploit the immunosuppressive properties of a transforming growth factor beta (TGF-\u03b2) mimic repurposed from helminths for cell type\u2013specific therapeutic \u201csilencing\u201d, as a new approach to complement existing therapies. Mouse CD4\u207a and CD8\u207a T cell\u2013targeted TGF-\u03b2 agonists selectively and potently silence antigen-specific T cell responses in OVA-immunized mice by suppressing pro-inflammatory effector, cytotoxic, and T follicular helper programs, while skewing cells toward a quiescent state biased toward regulatory and type 17 T cell phenotypes. Similarly, human CD4\u207a and CD8\u207a T cell\u2013targeted TGF-\u03b2 agonists precisely and effectively suppress live-attenuated influenza vaccine (LAIV)-induced T cell activation and expansion in human spleen organoids. Correspondingly, CD4\u207a T cell-targeted TGF-\u03b2 agonist effectively ameliorated disease activity and promoted disease remission in CD4\u207a T cell-driven models of autoimmune neuroinflammation and allergic airway inflammation, demonstrating efficacy in both prophylactic and established inflammatory settings. Moreover, both CD4\u207a and CD8\u207a T cell-targeted TGF-\u03b2 agonists ameliorated disease activity in graft-versus-host disease. Additionally, a human CD19\u207a B cell\u2013targeted TGF-\u03b2 agonist robustly inhibits germinal center B cell-to-plasmablast maturation and antibody responses in LAIV-stimulated human spleen organoids. These early-stage results suggest that cell-selective TGF-\u03b2 agonism merits further investigation as a versatile therapeutic approach for the precise silencing of pathogenic adaptive immune responses.<\/jats:p>","DOI":"10.64898\/2026.01.19.700410","type":"posted-content","created":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T18:00:11Z","timestamp":1768932011000},"source":"Crossref","is-referenced-by-count":0,"title":["Selective Immune Silencing by Targeted TGF-\u03b2 Mimics"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1220-3388","authenticated-orcid":false,"given":"Qinli","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masato","family":"Ogishi","sequence":"additional","affiliation":[{"name":"Institute for Immunity, Transplantation, and Infection, Department of 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