BPI overexpression suppresses Treg differentiation and induces exosome-mediated inflammation in systemic lupus erythematosus
Huai‐Chia Chuang, Ming‐Han Chen, Yi‐Ming Chen, Huang‐Yu Yang, Yi‐Ru Ciou, Chia‐Hsin Hsueh, Ching‐Yi Tsai, Tse‐Hua Tan
Abstract
BPI is a negative regulator of Treg differentiation. BPI overexpression in T-cell-derived exosomes or peripheral blood T cells may be a biomarker and pathogenic factor for human SLE nephritis, hepatitis, and arthritis.
Topics & Concepts
MicrovesiclesLupus nephritisCD86ExosomeInflammationImmunologyArthritisT cellDownregulation and upregulationMedicineCancer researchChemistryImmune systemInternal medicinemicroRNAGeneDiseaseBiochemistrySystemic Lupus Erythematosus ResearchExtracellular vesicles in diseaseRenal Diseases and Glomerulopathies