Loss of FOXP3+ CD25+ Tregs is independent of type I interferon signaling in lupus-prone mice

Abstract Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by deposition of autoantibodies that leads to tissue damage and inflammation. Our lab has generated the ARE mice strain low, chronic levels IFNg lupus-like disease. Regulatory T cells (Tregs) play important role in preventing autoimmunity suppressing cell activation, making them therapeutic target. In addition, type I interferon (IFN) also been broadly implicated SLE but its specific effect on Tregs remain unknown. To address impact a IFN signature dynamics regulatory (Tregs), we investigated marker expression receptor (IFNAR)-deficient mice. Single suspensions harvested from spleens kidneys −/−, IFNAR −/−/ARE −/−female between 150 200 days old were stained with panel markers associated Treg function for analysis flow cytometry. spleen, proportion CD4+ FOXP3+ expressing CD25 (IL2Ra) decreased −/−and not compared wild (wt). Thus, progression may be due loss bona fide population (FOXP3+ CD25+), as IL-2 contributes Tregs’ expansion function. Furthermore, −/−experienced increased CD4 infiltration well similar decrease FOX3+ CD25+ Tregs, which might explain inflammation kidneys. IFNg-mediated appears downregulate independent signaling. Future experiments aim perform vitroassays compare suppressive ability without CD25.