Chinese Journal of Dermatology ›› 2009, Vol. 42 ›› Issue (7): 470-472.

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Peripheral blood mononuclear cells (PBMCs) from patients with systemic lupus erythematosus mediate the adhesion of T lymphocytes to endothelial cells

  

  • Received:2008-07-01 Revised:2009-02-11 Online:2009-07-15 Published:2009-07-08

Abstract:

Objective To observe whether peripheral blood mononuclear cells (PBMCs) from patients with active systemic lupus erythematosus (SLE) can induce the adhesion of T lymphocytes to endothelial cells. Methods Sera and PBMCs were obtained from patients with active SLE and normal human controls. PBMCs were cultivated and culture supernatants were harvested. Human umbilical vein endothelial cells (HUVECs) were cultured in vitro with or without the presence of the sera or culture supernatants of PBMCs. Some cells were pretreated with the antibody to IL-17 before the treatment with the sera or supernatants. After another 48-hour culture, RT-PCR and real-time PCR were used to detect the mRNA expressions of adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-cadherin in HUVECs, wound healing assay to estimate the motility of HUVECs. Additionally, T lymphocytes were added to HUVECs 48 hours after stimulation with the sera or supernatants, the adhering of T lymphocytes to HUVECs was observed by microscopy. Results After stimulation with supernatants of PBMCs from patients with active SLE, the mRNA expressions of ICAM-1, VCAM-1 and E-cadherin were significantly increased in HUVEC, while the increase could be inhibited by the antibody to IL-17. The elevation of adhesion molecule expression subsequently promoted the motility of HUVEC, mediated the adhesion of T lymphocytes to HUVEC, and the antibody to IL-17 could suppress the adhesion of T lymphocytes and motility of HUVEC. Conclusion The culture supernatants of PBMCs from patients with active SLE can induce the expression of vascular cell adherin molecules and promote the adherin of T lymphocytes, which may in turn mediate the development of lupus vasculitis.