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Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Biomed+Res 2018 ; 32 (2): 113-22 Nephropedia Template TP
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Pathological significance and regulatory mechanism of lymphotoxin ? receptor overexpression in T cells of patients with systemic lupus erythematosus #MMPMID28963441
Yin C; Cai X; Wang H; Gu B; Yang X; Zhang R; Ji X
J Biomed Res 2018[Mar]; 32 (2): 113-22 PMID28963441show ga
Systemic lupus erythematosus (SLE) is a typical autoimmune disease. Lymphotoxin ? receptor (LT?R) signaling plays an important role in autoimmune inflammations. LT?R-Ig fusion protein, LT?R blocking agent, has been used to treat SLE, while its mechanism remains to be fully elucidated. In this study, to investigate the expression of LT?R 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 LT?R by flow cytometry and RNA assay. T cells were also stimulated with LIGHT, a ligand of LT?R, and then detected for their LT?R expressions and apoptosis by flow cytometry. Also, their expressions of inflammatory factors and receptors were determined by RNA assay. The results showed that LT?R positive cells were 22.75%±6.98% in CD3+ cells of SLE patients, while there were almost no LT?R positive cells in CD3+ cells of normal persons. Moreover, LT?R 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 LT?R, IL-23R and IL-17A, and apoptosis of T cells. In conclusion, we demonstrated a high expression of LT?R in the T cells of SLE patients which may be associated with pathogenesis of SLE.