Lymphocyte-endothelium interaction in systemic sclerosis and Raynaud's phenomenon

S. Della Bella, M. Molteni, C. Mocellin, S. Fumagalli, P. Bonara, R. Scorza

Research output: Contribution to journalArticlepeer-review

Abstract

Objective. To investigate interactions of immune cells with vascular endothelium in patients with systemic sclerosis (SSc) and in patients with idiopathic or autoimmune Raynaud's phenomenon (RP). Methods. Lymphocytes obtained from 11 patients with SSc, 9 with RP and 14 control subjects were pre-stimulated in vitro with alloantigens and cultured together with human umbilical vein endothelial cells (HUVECs). Lymphocyte adhesion and induction of endothelial HLA-class II molecules were measured by flow cytometry. Lymphocyte cytotoxicity against HUVECs was also evaluated. In some cases cells were cultured under experimental conditions of hypoxia and reoxygenation. Results. Lymphocyte adhesion and induction of endothelial cell expression of HLA-DR molecules were similar in controls and SSc patients, but significantly lower in RP (p <0.05 and p <0.03, respectively). Cytotoxic activity of lymphoblasts against endothelial cells was negligible in all patient groups. Under experimental conditions of hypoxia and reoxygenation lymphocyte adhesion was significantly greater than in normoxic conditions in SSc patients, while it was similar to normoxia in control subjects and RP patients. Conclusion. These results suggest that in RP patients there may be regulatory mechanisms of lymphocyte response able to control the processes that lead to lymphocyte adhesion and endothelial HLA-DR molecule induction. These mechanisms could play an important role in RP, and might possibly be lost in clinically evident SSc.

Original languageEnglish
Pages (from-to)647-654
Number of pages8
JournalClinical and Experimental Rheumatology
Volume19
Issue number6
Publication statusPublished - 2001

Keywords

  • Endothelial cells
  • Hypoxia
  • Lymphocytes
  • Raynaud's phenomenon
  • Systemic sclerosis

ASJC Scopus subject areas

  • Rheumatology
  • Immunology

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