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Naslov:HLA-DR–expressing fibroblast-like synoviocytes are inducible antigen presenting cells that present autoantigens in Lyme arthritis
Avtorji:ID Rouse, Joseph R. (Avtor)
ID Danner, Rebecca (Avtor)
ID Wahhab, Amanda (Avtor)
ID Pereckas, Michaela (Avtor)
ID Nguyen, Christine (Avtor)
ID McClune, Mecaila E. (Avtor)
ID Steere, Allen C. (Avtor)
ID Strle, Klemen (Avtor)
ID Jutras, Brandon L. (Avtor)
ID Lochhead, Robert B. (Avtor), et al.
Datoteke:.pdf PDF - Predstavitvena datoteka, prenos (2,14 MB)
MD5: EEE48FBBB463530321950D5E44A26A90
 
URL URL - Izvorni URL, za dostop obiščite https://acrjournals.onlinelibrary.wiley.com/doi/full/10.1002/acr2.11710
 
Jezik:Angleški jezik
Tipologija:1.01 - Izvirni znanstveni članek
Organizacija:Logo UKC LJ - Univerzitetni klinični center Ljubljana
Povzetek:Objective: HLA-DR–expressing fibroblast-like synoviocytes (FLS) are a prominent cell type in synovial tissue in chronic inflammatory forms of arthritis. FLS-derived extracellular matrix (ECM) proteins, including fibronectin-1 (FN1), contain immunogenic CD4+ T cell epitopes in patients with postinfectious Lyme arthritis (LA). However, the role of FLS in presentation of these T cell epitopes remains uncertain. Methods: Primary LA FLS and primary murine FLS stimulated with interferon gamma (IFNγ), Borrelia burgdorferi, and/or B burgdorferi peptidoglycan (PG) were assessed for properties associated with antigen presentation. HLA-DR–presented peptides from stimulated LA FLS were identified by immunopeptidomics analysis. OT-II T cells were co-cultured with stimulated murine FLS in the presence of cognate ovalbumin antigen to determine the potential of FLS to act as inducible antigen presenting cells (APCs). Results: FLS expressed HLA-DR molecules within inflamed synovial tissue and tendons from patients with postinfectious LA in situ. Major histocompatibility complex (MHC) class II and co-stimulatory molecules were expressed by FLS following in vitro stimulation with IFNγ and B burgdorferi and presented both foreign and self-MHC-II peptides, including an immunogenic T cell epitope derived from Lyme autoantigen FN1. Stimulated FLS induced proliferation of naive OT-II CD4+ T cells that were dependent on OT-II antigen and CD40. Stimulation with B burgdorferi PG enhanced FLS-mediated T cell activation. Conclusion: MHC-II+ FLS are inducible APCs that can induce CD4+ T cell activation in an antigen- and CD40-dependent manner. Activated FLS can also present ECM-derived Lyme autoantigens, implicating FLS in amplifying tissue-localized autoimmunity in LA.
Ključne besede:Lyme arthritis, autoimmune diseases, infectious disease
Status publikacije:Objavljeno
Verzija publikacije:Objavljena publikacija
Leto izida:2024
Št. strani:str. 678-689
Številčenje:Vol. 6, issue 10
PID:20.500.12556/DiRROS-29643 Novo okno
UDK:616.9
ISSN pri članku:2578-5745
DOI:10.1002/acr2.11710 Novo okno
COBISS.SI-ID:279250691 Novo okno
Opomba:Nasl. z nasl. zaslona; Opis vira z dne 25. 5. 2026;
Datum objave v DiRROS:02.06.2026
Število ogledov:88
Število prenosov:49
Metapodatki:XML DC-XML DC-RDF
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Gradivo je del revije

Naslov:ACR open rheumatology
Skrajšan naslov:ACR open rheumatol.
Založnik:John Wiley & Sons Inc.
ISSN:2578-5745
COBISS.SI-ID:529833497 Novo okno

Gradivo je financirano iz projekta

Financer:NIH - National Institutes of Health
Številka projekta:1R21AI148982-01
Naslov:MHC class II presentation of Borrelia burgdorferi and synovial tissue antigens in murine Lyme arthritis

Financer:NIH - National Institutes of Health
Številka projekta:1R01AI173256-01
Naslov:Defining the host and pathogen determinants of peptidoglycan induced pathophysiology in Lyme disease

Financer:NIH - National Institutes of Health
Številka projekta:1R01AI178711-01
Naslov:The natural release of unusual peptidoglycan fragments drives persistent Lyme disease symptoms in susceptible hosts

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Licenca:CC BY-NC 4.0, Creative Commons Priznanje avtorstva-Nekomercialno 4.0 Mednarodna
Povezava:http://creativecommons.org/licenses/by-nc/4.0/deed.sl
Opis:Licenca Creative Commons, ki prepoveduje komercialno uporabo, vendar uporabniki ne rabijo upravljati materialnih avtorskih pravic na izpeljanih delih z enako licenco.

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