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Association of Serum T cell Immunoglobulin Domain and Mucin-3 and Interleukin-17 with Systemic Lupus Erythematosus

Lairun Jin, Ran Bai, Jun Zhou, Wei Shi, Liang Xu, Jun Sheng, Hui Peng, Yuelong Jin, Hui Yuan

School of Public Health, Wannan Medical College, Wuhu, Anhui, China (mainland)

Med Sci Monit Basic Res 2018; 24:168-176

DOI: 10.12659/MSMBR.910949

Available online: 2018-10-23

Published: 2018-10-23


BACKGROUND: Previous studies have shown that T cell immunoglobulin domain and mucin-3 (Tim-3) and interleukin-17 (IL-17) are implicated in the development of several autoimmune diseases. However, it is unclear whether these proteins contribute to the pathogenesis of systemic lupus erythematosus (SLE). The purpose of this study was to evaluate SLE patient serum Tim-3 and IL-17 levels, and to assess correlations between these proteins and major clinical parameters of SLE.
MATERIAL AND METHODS: Overall, 55 SLE patients and 55 healthy controls were recruited in a case-control study. Serum Tim-3 and IL-17 levels were quantified using an enzyme-linked immunosorbent assay (ELISA) kit.
RESULTS: Serum Tim-3 and IL-17 levels in SLE patients were significantly elevated relative to healthy controls (all P<0.05). Serum Tim-3 levels were significantly lower in SLE patients with nephritis than in those SLE without nephritis (P<0.05), while no statistically significant correlation between serum IL-17 and nephritis was detected (P>0.05). Serum Tim-3 with IL-17 levels were positively correlated in SLE patients (rs=0.817, P<0.01); however, no statistically significant correlation was found between serum Tim-3 or IL-17 levels and systemic lupus erythematosus disease activity index (SLEDAI) scores in those with SLE (all P>0.05). In addition, serum Tim-3 was associated with central lesions in SLE patients, while there were no significant correlations between serum Tim-3 or IL-17 levels and other SLE clinical parameters.
CONCLUSIONS: Increased serum Tim-3 and IL-17 levels and their clinical associations in SLE patients suggest their possible role in this disease.

Keywords: Immunoglobulin Allotypes, Interleukin-17, Lupus Vasculitis, Central Nervous System