Title: Pathological Significance and Regulatory Mechanism of Abnormal High Expression of Lymphotoxin β Receptor in T cells of Patients with Systemic Lupus Erythematosus
Authors: Cheng Yin, Huijuan Wang, Bingjie Gu, Xiaofan Yang, Rong Zhang, Xiaohui Ji
Institutions: Department of Microbiology and Immunology, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Abstract: Systemic lupus erythematosus is a typical autoimmune disease. Lymphotoxin β receptor is a member of tumor necrosis factor receptor superfamily. Recent studies have found that LTβR signal played an important role in the occurrence of chronic inflammation and pathogenic autoimmune. Our research found that peripheral blood T cells of SLE patients highly expressed LTβR, promoting large amount of apoptosis of T cells, inhibiting replication and differentiation of T cells, and leading to the change of the ratio of T and B cells; at the same time, with abnormal high expression of LTβR and its ligand, the intracellular signal in the patients' T cells was enhanced, which promoted the expression of IL-23R and increased the sensitivity of T cells to differentiating into Th17 cells. The increased number of pathogenic Th-17 cells,might participate in the pathogenesis of SLE.
Keywords: Pathogenic mechanisms of SLE; LTβR; TH-17; IL-23R
Full Text: PDFJBR-2013-0046.pdf
J Biomed Res published on June 30th, 2013, doi:10.7555/JBR.27. 20130046