Treg derived Amphiregulin protects from murine lupus nephritis via tissue reparative effects.

ABSTRACT: Systemic lupus erythematosus (SLE) is a common autoimmune disease that affects multiple organ systems. Among the most severe manifestations of SLE is lupus nephritis (LN), which causes particularly high morbidity. Recently, we identified amphiregulin (AREG), an epidermal growth factor receptor ligand, as a key mediator of LN via downregulation of pathogenic CD4⁺ T-cell responses. In human LN, AREG is mainly produced by regulatory T cells (Tregs) and monocytes/macrophages (M/M). Since AREG´s functions have been shown to vary considerably depending on the source, we aimed to clarify the cell-type-specific roles of AREG using the pristane model of LN. Conditional knockout mice lacking Treg- but not M/M-derived AREG showed worse LN outcome at 12 and 15 months with increased glomerul

SUBMITTER: Ehnold LI 

PROVIDER: S-EPMC11882795 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature