STING/type I interferon pathway is required for antigen-containing PLGA nanoparticle- and apoptotic cell-induced CD4+ T cell tolerance.

ABSTRACT: Autoreactive CD4⁺ T cell infiltration, tissue destruction, and spread epitope-specific CD4⁺ T cell activation underly CD4⁺ T cell-mediated autoimmune disease pathogenesis. Here, we identify previously unknown pathways required for antigen (Ag)-specific tolerogenic immune-modifying particle/Cour nanoparticle (TIMP/CNP)-induced tolerance. The data show that myeloid cells phagocytose CNPs, undergo apoptosis, and release oxidized DNA [8-hydroxy-2'-deoxyguanosine (8-OHG)]. Subsequently, Ag-specific CNP treatment increases the number of PD-L1⁺ cDC2 dendritic cells and the number of FoxP3⁺, CTLA-4⁺, PD-1⁺, and IL-10⁺ regulatory CD4⁺ T cells via a stimulator of interferon genes (STING)/interferon-α/β

SUBMITTER: Podojil JR 

PROVIDER: S-EPMC12758558 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature