Oxidized LDL induces in vitro lymphocyte activation in antiphospholipid syndrome

Renata Laczik, Peter Szodoray, Katalin Veres, Gabriella Lakos, Sandor Sipka, Gyula Szegedi, Pal Soltész

Research output: Article

7 Citations (Scopus)

Abstract

Oxidized low-density lipoprotein (oxLDL) is a key feature of the atheromatosus plaque and plays a critical role in foam cell formation and perpetuation of inflammatory processes. In antiphospholipid syndrome (APS), oxLDL molecules form complexes with β2GPI and become target antigens for autoantibodies, which are detectable in the sera of these patients. oxLDL takes part in the pathogenesis of APS and in the concomitant accelerated atherosclerosis, yet the exact associated immune mechanisms are not clear in details. The aim of this study was to assess the activation and proliferation response of peripheral blood mononuclear cells (PBMCs) derived from patients with APS in the presence of oxLDL. Thirteen patients with APS and nine healthy individuals were enrolled in the study. Separated PBMCs of these patients were cultured in the presence of immunogenic epitope of oxLDL. Lymphocyte proliferation and cytokine secretion (TNF-α, IL-2, IFN-γ, IL-4, and IL-10) were assessed by ELISA. We found significant PBMC proliferation in APS compared to healthy controls (PI/proliferation index/APS: 1.76 vs. PI control: 0.56; p = 0.032). A significant IL-2 and IFN-γ secretion were detected upon oxLDL stimulus in patients with APS compared to controls (IL-2 cytokine secretion index (CSI) APS: 278.5, IL-2 CSI controls: 65.1; p = 0.025; IFN-γ CSI APS: 163.2, IFN-γ CSI controls: 77.4; p = 0.025). Based on our findings, we assume that oxLDL via Th1-type cytokine production and lymphocyte proliferation may contribute to the perpetuation of immune processes in APS.

Original languageEnglish
Pages (from-to)334-339
Number of pages6
JournalAutoimmunity
Volume43
Issue number4
DOIs
Publication statusPublished - jún. 1 2010

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ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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