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Aetiopathogenesis

 

Reduced non-switched memory B cell subsets cause imbalance in B cell repertoire in systemic sclerosis


1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11

 

  1. Department of Immunology and Biotechnology, University of Pécs, Clinical Center, Pécs, Hungary.
  2. Department of Immunology and Biotechnology, University of Pécs, Clinical Center, Pécs, Hungary.
  3. Department of Immunology and Biotechnology, University of Pécs, Clinical Center, Pécs, Hungary.
  4. Department of Immunology and Biotechnology, University of Pécs, Clinical Center, Pécs, Hungary.
  5. Department of Immunology and Biotechnology, University of Pécs, Clinical Center, Pécs, Hungary.
  6. Department of Immunology and Biotechnology, University of Pécs, Clinical Center, Pécs, Hungary.
  7. Institute of Bioanalysis, University of Pécs, Medical School, Pécs, Hungary.
  8. Department of Rheumatology and Immunology, University of Pécs, Clinical Center, Pécs, Hungary.
  9. Department of Rheumatology and Immunology, University of Pécs, Clinical Center, Pécs, Hungary.
  10. Department of Rheumatology and Immunology, University of Pécs, Clinical Center, Pécs, Hungary.
  11. Department of Immunology and Biotechnology, University of Pécs, Clinical Center, Pécs, Hungary. berki.timea@pte.hu

CER8819
2016 Vol.34, N°5 ,Suppl.100
PI 0030, PF 0036
Aetiopathogenesis

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PMID: 27056741 [PubMed]

Received: 28/07/2015
Accepted : 04/12/2015
In Press: 08/04/2016
Published: 13/10/2016

Abstract

OBJECTIVES:
Analysis of peripheral blood B lymphocytes in patients with systemic sclerosis (SSc) has provided evidence for specific alterations in naive and memory B cell balance. However, memory B cell subsets in SSc have not been thoroughly investigated. This study sought to identify phenotypic abnormalities and activation markers in peripheral blood memory B cells in SSc subtypes.
METHODS:
Blood samples were obtained from 28 SSc patients with early form of disease (9 limited (lcSSc), 19 diffuse cutaneous SSc (dcSSc)) and 15 healthy controls. After magnetic bead separation of CD19+ B cells, multiparametric flow cytometry was performed and CD19+CD27- IgD+ naive, CD19+CD27+ memory, CD19+CD27+IgD+ non-switched memory CD19+CD27+IgD- switched memory, CD19+CD27-IgD- double negative (DN) memory, CD80+ or CD95+ activated cells were identified.
RESULTS:
The proportion of naive B cells was higher (p=0.046) in SSc than in controls, with a decreased percentage of memory (p=0.018), especially non-switched memory B cells (p=0.015). The dcSSc patients had a significantly higher frequency of switched memory and DN memory B cells compared to lcSSc patients (p=0.025 and p=0.031). Percentage of CD95+CD27+ memory and CD95+ DN memory B cells was also significantly elevated in dcSSc compared to lcSSc patients (p=0.038 and p=0.045).
CONCLUSIONS:
We conclude that the decreased proportion of memory B cells in SSc is due to reduction of non- switched memory B cells, resulting in an imbalance between the tolerogenic and activated memory B cell types. Elevated switched and activated CD95+ DN memory B cells may serve as a biomarker for dcSSc and can have a pathogenic potential by cytokine and autoantibody production.

Rheumatology Article