Systemic lupus erythematosus（SLE） is a typical autoimmune disease. Lymphotoxin β receptor（LTβR） signaling plays an important role in autoimmune inflammations. LTβR-Ig fusion protein, LTβR blocking agent, has b...Systemic lupus erythematosus（SLE） is a typical autoimmune disease. Lymphotoxin β receptor（LTβR） signaling plays an important role in autoimmune inflammations. LTβR-Ig fusion protein, LTβR blocking agent, has been used to treat SLE, while its mechanism remains to be fully elucidated. In this study, to investigate the expression of LTβR in the T cells of SLE patients and its roles in the pathogenesis of SLE, we isolated the peripheral blood T cells of SLE patients and normal controls to detect expression of LTβR by flow cytometry and RNA assay. T cells were also stimulated with LIGHT, a ligand of LTβR, and then detected for their LTβR expressions and apoptosis by flow cytometry. Also, their expressions of inflammatory factors and receptors were determined by RNA assay. The results showed that LTβR positive cells were 22.75%±6.98% in CD3~＋ cells of SLE patients, while there were almost no LTβR positive cells in CD3~＋ cells of normal persons. Moreover, LTβR expression was remarkably higher in CD3,CD4 and CD8 positive T cells of active SLE patients than non/low active patients（all P〈0.05）, and positively correlated with increased Ig level, decreased complement level and renal damage. Moreover, the stimulation of SLE T cells with LIGHT promoted higher expression of LTβR, IL-23 R and IL-17 A, and apoptosis of T cells. In conclusion,we demonstrated a high expression of LTβR in the T cells of SLE patients which may be associated with pathogenesis of SLE.展开更多
文摘Systemic lupus erythematosus（SLE） is a typical autoimmune disease. Lymphotoxin β receptor（LTβR） signaling plays an important role in autoimmune inflammations. LTβR-Ig fusion protein, LTβR blocking agent, has been used to treat SLE, while its mechanism remains to be fully elucidated. In this study, to investigate the expression of LTβR in the T cells of SLE patients and its roles in the pathogenesis of SLE, we isolated the peripheral blood T cells of SLE patients and normal controls to detect expression of LTβR by flow cytometry and RNA assay. T cells were also stimulated with LIGHT, a ligand of LTβR, and then detected for their LTβR expressions and apoptosis by flow cytometry. Also, their expressions of inflammatory factors and receptors were determined by RNA assay. The results showed that LTβR positive cells were 22.75%±6.98% in CD3~＋ cells of SLE patients, while there were almost no LTβR positive cells in CD3~＋ cells of normal persons. Moreover, LTβR expression was remarkably higher in CD3,CD4 and CD8 positive T cells of active SLE patients than non/low active patients（all P〈0.05）, and positively correlated with increased Ig level, decreased complement level and renal damage. Moreover, the stimulation of SLE T cells with LIGHT promoted higher expression of LTβR, IL-23 R and IL-17 A, and apoptosis of T cells. In conclusion,we demonstrated a high expression of LTβR in the T cells of SLE patients which may be associated with pathogenesis of SLE.
