Background TAM (Tyro3, Axl, Mer) kinases receptors and Gas6 ligand are pivotal regulators of innate immunity and responsible for the clearance of apoptotic cells. TAM receptors and Gas6 ligand were individually tested in adult onset lupus with different results.1-5
Objectives To quantify simultaneously soluble TAM receptors and Gas6 ligand in JSLE patients and evaluated the relation with disease activity parameters.
Methods sTyro3, sAxl, sMer and Gas6 ligand were measured in sera from 44 JSLE patients (39 girls, mean age 14.2 yrs, ACR criteria), 14 gender and age-matched healthy individuals (11 girls, mean age 13.9 yrs) and 9 JIA patients as disease controls (4 girls, mean age 10.5, ACR criteria). Soluble TAM receptors and Gas6 ligand were quantified by commercial ELISA Kits following manufacturer's instructions. Disease activity parameters included SLEDAI score, anti-dsDNA (ELISA), C3 and C4 (nephelometry), ERS (Westergreen) and CRP (nephelometry). Fifteen JSLE patients had active disease (SLEDAI score >4) and 34 had nephritis. Statistical analysis used Mann-Whitney U test and Spearman's rank. A p<0.05 was considered significant.
Results sTyro3, sAxl, sMer and Gas6 ligand were detected in all patients and controls with results similar to that described in literature. JSLE patients presented sTyro3, sAxl, sMer and Gas6 ligand levels similar to healthy controls and patients with active disease and with nephritis had the higher levels, but without statistical significance. TAM receptors and Gas6 ligand levels did not correlated with disease activity parameters. JIA patients had soluble levels similar to healthy controls. (Table)
Conclusions To our knowledge this is the first study to quantify soluble TAM (Tyro3, Axl, Mer) receptors and Gas6 ligand in JSLE patients. Although most studies with adult onset LES have reported increased concentrations this was not observed in JSLE patients even when we considered patients with active disease and with nephritis. Further studies with exclusively JSLE patients are needed to confirm these results.
Zhu H, et al. Lupus 2014;23:624-34.
Recarte-Perlz P, et al. Arthritis Res Ther 2013;15:R41.
Gheita TA, et al. J Clin Immunol. 2012;32:1279-86.
Wu J, et al. Arthritis Res Ther 2011;13:R62.
Suh CH, et al. Arthritis Res Ther. 2010;12:R146.
Acknowledgements We thank FAPESP (grants 2012/22997-4 and 2008/58238-4) for supporting this study.
Disclosure of Interest None declared