AB0134 SERUM LL-37, GALECTIN-3, AND TOLL-LIKE RECEPTORS-3 LEVELS DECREASE IN PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS

Abstract

Background:Systemic lupus erythematosus (SLE) is a systemic inflammatory disease characterized by heterogeneous clinical manifestations (1). Although there are significant developments with its pathogenesis, it is still not fully known. In recent years, pathways such as NETosis and plasmacytoid dendritic cell (pDC) activation have been emphasized in the pathogenesis of SLE (2, 3).Objectives:In our study, we aimed to investigate serum LL-37, Galectin-3, and Toll-like receptors-3 (TLR)-3 levels, which are thought to be related to pathogenetic pathways in SLE patients.Methods:17 SLE patients and 33 healthy controls were included in the study. The clinical and laboratory features of the patients were determined. Serum LL-37, Galectin-3, and TLR-3 levels were determined by ELISA (enzyme-linked immunosorbent assay) method using the appropriate commercial kit, and the results were evaluated according to the manufacturer’s instructions.Results:The clinical and laboratory features of the groups are described in Table 1. In our study, serum LL-37, Galectin-3, and TLR-3 levels were decreased statistically significantly in SLE patients compared to healthy control (p = 0.007, p = 0.002, and p = 0.008, respectively).Table 1.Clinical and laboratory features of the groups in the studyHealthy control (n=33)SLE(n=17)pAge (years)34.1 ± 3.740 ± 11.40.05Sex (n; female/male)33/017/0LL-37(ng/ml)78.6 ± 92.614.2 ± 19.30.007Galectin-3 (ng/ml)25.5 ± 23.26.7 ± 7.60.002Toll-like receptors-3 (pg/ml)7893.4 ± 1041.3916.2 ± 469.70.008Conclusion:It is suggested that LL-37, galectin-3, and TLR-3 levels have various effects on NEtosis and pDc activation pathways in SLE pathogenesis. In our study, low levels of serum LL-37, galectin-3, and TLR-3 in SLE patients suggest that they are associated with SLE pathogenesis.References:[1]Aringer M, Schneider M. [Systemic lupus erythematosus]. Dtsch Med Wochenschr.2016;141:537-43.[2]Panda SK, Kolbeck R, Sanjuan MA. Plasmacytoid dendritic cells in autoimmunity. Curr Opin Immunol. 2017;44:20-25.[3]van der Linden M, van den Hoogen LL, Westerlaken GHA, Fritsch-Stork RDE, van Roon JAG, Radstake TRDJ, Meyaard L. Neutrophil extracellular trap release is associated with antinuclear antibodies in systemic lupus erythematosus and anti-phospholipid syndrome. Rheumatology (Oxford). 2018;57:1228-1234.Disclosure of Interests:None declared