ArticlePloS one2010
Comparative proteomic analysis of serum from patients with systemic sclerosis and sclerodermatous GVHD. Evidence of defective function of factor H.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- The local complement activation on vascular bed of patients with systemic sclerosis: a hypothesis-generating study.PloS one · 2015Trial
- Multi-omic analysis identifies biological processes underlying progressive interstitial lung disease in systemic sclerosis.The FEBS journal · 2025Article
- Hemostasis and complement in allogeneic hematopoietic stem cell transplantation: clinical significance of two interactive systems.Bone marrow transplantation · 2024Review
- Beyond Systemic Lupus Erythematosus and Anti-Phospholipid Syndrome: The Relevance of Complement From Pathogenesis to Pregnancy Outcome in Other Systemic Rheumatologic Diseases.Frontiers in pharmacology · 2022Review
- Innate immune response in systemic autoimmune diseases: a potential target of therapy.Inflammopharmacology · 2020Review
- Complement in Thrombotic Microangiopathies: Unraveling Ariadne's Thread Into the Labyrinth of Complement Therapeutics.Frontiers in immunology · 2019Review
- Innate Immunity in Systemic Sclerosis.Current rheumatology reports · 2017Review
- The primary care physician in the early diagnosis of systemic sclerosis: the cornerstone of recognition and hope.The American journal of the medical sciences · 2014Review
- Complement in the immunopathogenesis of rheumatic disease.Nature reviews. Rheumatology · 2012Review
- Proteomics approaches to fibrotic disorders.Fibrogenesis & tissue repair · 2012Article
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSystemic sclerosis (SSc) is an autoimmune disease characterized by immunological and vascular abnormalities. Until now, the cause of SSc remains unclear. Sclerodermatous graft-versus-host disease (ScGVHD) is one of the most severe complications following bone marrow transplantation (BMT) for haematological disorders. Since the first cases, the similarity of ScGVHD to SSc has been reported. However, both diseases could have different etiopathogeneses. The objective of this study was to identify new serum biomarkers involved in SSc and ScGVHD. METHODOLOGY: Serum was obtained from patients with SSc and ScGVHD, patients without ScGVHD who received BMT for haematological disorders and healthy controls. Bi-dimensional electrophoresis (2D) was carried out to generate maps of serum proteins from patients and controls. The 2D maps underwent image analysis and differently expressed proteins were identified. Immuno-blot analysis and ELISA assay were used to validate the proteomic data. Hemolytic assay with sheep erythrocytes was performed to evaluate the capacity of Factor H (FH) to control complement activation on the cellular surface. FH binding to endothelial cells (ECs) was also analysed in order to assess possible dysfunctions of this protein. PRINCIPAL
findingsFourteen differentially expressed proteins were identified. We detected pneumococcal antibody cross-reacting with double stranded DNA in serum of all bone marrow transplanted patients with ScGVHD. We documented higher levels of FH in serum of SSc and ScGVHD patients compared healthy controls and increased sheep erythrocytes lysis after incubation with serum of diffuse SSc patients. In addition, we observed that FH binding to ECs was reduced when we used serum from these patients.
conclusionsThe comparative proteomic analysis of serum from SSc and ScGVHD patients highlighted proteins involved in either promoting or maintaining an inflammatory state. We also found a defective function of Factor H, possibly associated with ECs damage.
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