Peripheral blood brain-derived neurotrophic factor level and tyrosine kinase B expression on T lymphocytes in systemic lupus erythematosus: Implications for systemic involvement

Abstract

ObjectiveBrain-derived neurotrophic factor (BDNF) has been reported to be involved in the pathogenesis of autoimmune diseases and tyrosine kinase B (TrkB) is the specific receptor for BDNF. Our aim in this study was to investigate serum BDNF level and TrkB expression on peripheral blood T cell surface in patients with systemic lupus erythematosus (SLE) and explore potential relationship between serum BDNF and SLE. MethodsSamples from fifty SLE patients and thirty healthy controls were evaluated. Serum BDNF level was measured by enzyme-linked immunosorbent assay (ELISA) and the percentages of TrkB expression on the surface of CD3 + CD4 + and CD3 + CD8 + T lymphocytes were measured by flow cytometry. The SLE patients were divided into subgroups according to whether they exhibited brain, kidney or lung involvement, and whether the disease was active or inactive. ResultsSerum BDNF levels in SLE patients were decreased when compared to the controls (p < 0.001). Comparing with the SLE individuals without systemic involvement, the BDNF levels were decreased in SLE patients with lupus nephritis (p = 0.042) and in SLE patients with neuropsychiatric manifestations (p = 0.04). On the other hand, the BDNF level was significantly increased in the inactive SLE group (p < 0.001) compared to the active SLE group. In addition, the percentages of TrkB expression on CD3 + CD4 + and CD3 + CD8 + T cell surface in SLE were significantly higher (p < 0.001; p < 0.001, respectively) than that in the controls. ConclusionsSerum BDNF level combined with TrkB expression on T cell surface can reflect SLE activity. It is possible that BDNF may be used as a potential serological biomarker for disease activity of SLE. In addition, the significant decrease in serum BDNF level may imply systemic involvement of SLE, as well as, possibly, differentiate neuropsychiatric SLE from hormone-induced mental disorders.