The threshold value of 70 AU was calculated using the 98th percentile around the OD reading for the control group. of some SLE patients, but their prevalence and significance have not been yet investigated. The aims of this study were to determine the prevalence of anti-ficolin-3 antibodies among SLE patients and to investigate their potential as diagnostic and/or prognostic biomarkers in SLE. In this retrospective study, sera from SLE patients (n = 165) were selected from a preexisting declared biological collection. Samples from healthy controls (n = 48) were matched with SLE sera. Disease activity was decided according to the SLEDAI score. Anti-ficolin-3, anti-dsDNA and anti-C1q antibodies levels were measured in sera by ELISA. First, a highly significant difference was found in the anti-ficolin-3 levels between SLE patients and healthy subjects. Anti-ficolin-3 antibodies were detected as positive in 56 of 165 (34%) SLE patients. The titer of anti-ficolin-3 antibodies was correlated with the SLEDAI score (r = 0.38, p<0.0001). The presence of anti-ficolin-3 antibodies was associated with anti-C1q and anti-dsDNA antibodies. Regarding associations with clinical manifestations, the presence of active lupus nephritis was significantly associated with the presence of anti-ficolin-3 antibodies (p0.001). This association with renal involvement was higher with anti-ficolin-3 or anti-C1q antibodies than with other auto-antibodies. Interestingly, the combination of anti-ficolin-3 and anti-C1q antibodies exhibited higher specificity than any other serological biomarker. These results suggest that anti-ficolin-3 antibodies could be useful for the diagnosis of active nephritis in SLE patients. Introduction Systemic lupus erythematosus (SLE) is usually a chronic autoimmune SR9011 hydrochloride disease with a prevalence of 4/10,000 among Northern Europeans and a predisposition of women of childbearing age [1]. SLE is usually characterized by the presence of circulating autoantibodies directed against self-antigens, such as dsDNA, nuclear antigens and several cytoplasmic components [2]. The accumulation of the resulting immune complexes mediates a systemic inflammatory response that is the primary cause of tissue damage. Recently, defects in apoptotic cells clearance leading to secondary cell necrosis and subsequent release of intracellular autoantigens has been proposed as one of the mechanisms of induction of these autoantibodies [3] [4]. According to this proposal, molecules worth focusing SR9011 hydrochloride on in the uptake of dying cells could possess a job in host safety against autoimmune illnesses, including SLE SR9011 hydrochloride [5] [6] [7] [8]. From its well characterized anti-microbial part Aside, the go with system in addition has a pivotal part in maintaining sponsor integrity through the elimination of apoptotic and broken cells aswell as by clearing circulating immune system complexes [9]. Certainly, zero early go with components tend to be associated with improved susceptibility to both attacks and autoimmune illnesses such as for example SLE, assisting a protective part for the go with system. Mice lacking for C1q, the reputation protein from the traditional go with pathway, are predisposed to SLE-like illnesses [10] and human being studies record that hereditary homozygous deficiencies of C1q are highly connected with susceptibility to SLE, having a defect in apoptotic cells uptake by macrophages in SLE individuals [11]. Recent reviews suggest a job for mannan-binding lectin (MBL), a reputation protein from the lectin go with pathway, in the pathogenesis of SLE [12]. Certainly, gene polymorphisms resulting in reduced degrees of serum MBL had been found connected with a predisposition to SLE [13]. Nevertheless, although MBL-null mice show faulty clearance of apoptotic cells, they neglect to develop symptoms of autoimmune illnesses, SR9011 hydrochloride suggesting the power of other substances to pay for Tmem34 MBL insufficiency [14]. The part of the lately determined complement-activating lectin-like protein ficolins (ficolin-1, and -3 -2, referred as M- also, L- and H-ficolins) continues to be suggested, since these protein may actually mediate immune effector functions just like those of C1q and MBL [14] [15]. Among these protein, Ficolin-3 deserves unique interest in the framework of autoimmunity because it was characterized like a serum antigen focus on (Hakata antigen) for an autoantibody within a Japanese individual with SLE [16]. Ficolin-3 offers poor lectin-like activity, as SR9011 hydrochloride demonstrated by glycan array testing, nonetheless it binds to acetylated albumin with high affinity [17] [18]. It.