Title: Pathological significance and regulatory mechanism of lympho-toxin β receptor overexpression in T cells of patients with systemic lupus erythematosus

 

Authors: Cheng Yin1,2, Xubing Cai2, Huijuan Wang1, Bingjie Gu3, Xiaofan Yang1, Rong Zhang1, Xiaohui Ji1

 

Institutions: 1Department of Immunology, Basic Medical School, Nanjing Medical University, Nanjing, Jiangsu 211166, China;2Red Cross Blood Center, Nanjing, Jiangsu 210003, China;3Rheumatology Department of Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, 210006, China.

 

Abstract: 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-23R and IL-17A, 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.

 

Keywords: lupus erythematosus, systemic (SLE), lymphotoxin β receptor (LTβR), interleukin-17 (IL-17), interleukin-23 receptor (IL-23R)

 

Full Text:JBR-2013-0046.pdf

 

J Biomed Res published on 30 June, 2013, doi:10.7555/JBR.27.20130046