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Disturbed Complement Receptor Expression Pattern of B Cells Is Enhanced by Toll-like Receptor CD180 Ligation in Diffuse Cutaneous Systemic Sclerosis.
Erdo-Bonyár, Szabina; Rapp, Judit; Subicz, Rovéna; Böröcz, Katalin; Szinger, Dávid; Filipánits, Kristóf; Minier, Tünde; Kumánovics, Gábor; Czirják, László; Berki, Tímea; Simon, Diána.
Afiliación
  • Erdo-Bonyár S; Department of Immunology and Biotechnology, Clinical Center, University of Pécs Medical School, H-7624 Pécs, Hungary.
  • Rapp J; Department of Immunology and Biotechnology, Clinical Center, University of Pécs Medical School, H-7624 Pécs, Hungary.
  • Subicz R; Department of Immunology and Biotechnology, Clinical Center, University of Pécs Medical School, H-7624 Pécs, Hungary.
  • Böröcz K; Department of Immunology and Biotechnology, Clinical Center, University of Pécs Medical School, H-7624 Pécs, Hungary.
  • Szinger D; Department of Immunology and Biotechnology, Clinical Center, University of Pécs Medical School, H-7624 Pécs, Hungary.
  • Filipánits K; Department of Rheumatology and Immunology, Clinical Center, University of Pécs Medical School, H-7632 Pécs, Hungary.
  • Minier T; Department of Rheumatology and Immunology, Clinical Center, University of Pécs Medical School, H-7632 Pécs, Hungary.
  • Kumánovics G; Department of Rheumatology and Immunology, Clinical Center, University of Pécs Medical School, H-7632 Pécs, Hungary.
  • Czirják L; Department of Rheumatology and Immunology, Clinical Center, University of Pécs Medical School, H-7632 Pécs, Hungary.
  • Berki T; Department of Immunology and Biotechnology, Clinical Center, University of Pécs Medical School, H-7624 Pécs, Hungary.
  • Simon D; Department of Immunology and Biotechnology, Clinical Center, University of Pécs Medical School, H-7624 Pécs, Hungary.
Int J Mol Sci ; 25(17)2024 Aug 26.
Article en En | MEDLINE | ID: mdl-39273179
ABSTRACT
Autoantibody production is a hallmark of systemic sclerosis (SSc) and the most extensively studied role of B cells in the pathogenesis of the disease. However, the potential involvement of innate immune molecules in B-cell dysfunction in SSc is less understood. B-cell activation is an early event in the pathogenesis of SSc and is influenced by complement receptors (CRs) and Toll-like receptors (TLRs), shaping antibody responses. CR2 and CR1 modulate B-cell activation, and the roles of CR3 and CR4 are associated with autoimmune conditions. We investigated the expression of CRs in B cells from patients with the more severe form of the disease, diffuse cutaneous SSc (dcSSc), and the effect of TLR CD180 ligation on their expression. We found no significant difference in the basal expression of CD21 and CD11c in B cells between dcSSc and healthy controls (HCs). However, reduced basal CD11b expression in B cells in dcSSc compared to HCs, accompanied by a decrease in CD35 and an increase in CD11c expression following CD180 ligation may promote plasma cell formation and autoantibody production. Additionally, we searched for correlations between dcSSc-associated anti-DNA topoisomerase I (Scl-70) autoantibody, anti-citrate synthase (CS) natural autoantibody and complement component 3 (C3) levels and found a negative correlation between C3 and anti-CS autoantibody in dcSSc but not in HCs, supporting the hypothesis that natural autoantibodies could activate the complement system contributing to tissue injury in SSc.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Autoanticuerpos / Linfocitos B / Receptores de Complemento Límite: Adult / Aged / Female / Humans / Male / Middle aged Idioma: En Revista: Int J Mol Sci Año: 2024 Tipo del documento: Article País de afiliación: Hungria Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Autoanticuerpos / Linfocitos B / Receptores de Complemento Límite: Adult / Aged / Female / Humans / Male / Middle aged Idioma: En Revista: Int J Mol Sci Año: 2024 Tipo del documento: Article País de afiliación: Hungria Pais de publicación: Suiza