| http://purl.uniprot.org/citations/34815797 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/34815797 | http://www.w3.org/2000/01/rdf-schema#comment | "Background: Serum-derived exosomes are correlated with disease severity of human systemic lupus erythematosus (SLE). The proteins in the T-cell-derived exosomes from SLE patients could contribute to inflammation. Methods: We characterized proteins of T cell-derived exosomes from SLE patients and healthy controls by proteomics. To study the potential pathogenic role of the identified exosomal protein, we generated and characterized T-cell-specific transgenic mice that overexpressed the identified protein in T cells using immunohistochemistry, immunoblotting, and single-cell RNA sequencing. Results: We identified an overexpressed protein, bactericidal/permeability-increasing protein (BPI), in SLE T cells and T-cell-derived exosomes. T-cell-specific BPI transgenic (Lck-BPI Tg) mice showed multi-tissue inflammation with early induction of serum IL-1β levels, as well as serum triglyceride and creatinine levels. Interestingly, exosomes of Lck-BPI Tg T cells stimulated IL-1β expression of wild-type recipient macrophages. Remarkably, adoptive transfer of BPI-containing exosomes increased serum IL-1β and autoantibody levels in recipient mice. The transferred exosomes infiltrated into multiple tissues of recipient mice, resulting in hepatitis, nephritis, and arthritis. ScRNA-seq showed that Lck-BPI Tg T cells displayed a decrease of Treg population, which was concomitant with ZFP36L2 upregulation and Helios downregulation. Furthermore, in vitro Treg differentiation was reduced by BPI transgene and enhanced by BPI knockout. Conclusions: 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."xsd:string |
| http://purl.uniprot.org/citations/34815797 | http://purl.org/dc/terms/identifier | "doi:10.7150/thno.63743"xsd:string |
| http://purl.uniprot.org/citations/34815797 | http://purl.uniprot.org/core/author | "Chen Y.M."xsd:string |
| http://purl.uniprot.org/citations/34815797 | http://purl.uniprot.org/core/author | "Tan T.H."xsd:string |
| http://purl.uniprot.org/citations/34815797 | http://purl.uniprot.org/core/author | "Yang H.Y."xsd:string |
| http://purl.uniprot.org/citations/34815797 | http://purl.uniprot.org/core/author | "Chen M.H."xsd:string |
| http://purl.uniprot.org/citations/34815797 | http://purl.uniprot.org/core/author | "Tsai C.Y."xsd:string |
| http://purl.uniprot.org/citations/34815797 | http://purl.uniprot.org/core/author | "Chuang H.C."xsd:string |
| http://purl.uniprot.org/citations/34815797 | http://purl.uniprot.org/core/author | "Hsueh C.H."xsd:string |
| http://purl.uniprot.org/citations/34815797 | http://purl.uniprot.org/core/author | "Ciou Y.R."xsd:string |
| http://purl.uniprot.org/citations/34815797 | http://purl.uniprot.org/core/date | "2021"xsd:gYear |
| http://purl.uniprot.org/citations/34815797 | http://purl.uniprot.org/core/name | "Theranostics"xsd:string |
| http://purl.uniprot.org/citations/34815797 | http://purl.uniprot.org/core/pages | "9953-9966"xsd:string |
| http://purl.uniprot.org/citations/34815797 | http://purl.uniprot.org/core/title | "BPI overexpression suppresses Treg differentiation and induces exosome-mediated inflammation in systemic lupus erythematosus."xsd:string |
| http://purl.uniprot.org/citations/34815797 | http://purl.uniprot.org/core/volume | "11"xsd:string |
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