Levels Of anti-C1q Antibodies Research Articles

Major low-energy trauma results in non-specific immunoglobulin generation without evidence for specific autoantibody production: A prospective cohort study.

Cellular debris resulting from large trauma might overwhelm the scavenger mechanisms and lead to autoimmune reactions. We analysed whether a major well-defined trauma in humans induces laboratory signs of transient autoimmunity in the months after the insult. We included 50 patients with pertrochanteric femur fracture undergoing intramedullary nail osteosynthesis in a prospective cohort study and followed them at 3-4 days, 6 weeks, 12 weeks and 12 months postoperatively. By standard techniques, we assessed levels of total immunoglobulins, anti-nuclear antibodies (ANA), anti-cardiolipin antibodies, anti-dsDNA antibodies and anti-C1q antibodies, as well as antibodies against cytomegalovirus (CMV) as a control. Blood leukocyte differential and lymphocyte subpopulations were determined at baseline and in the first two postoperative samples. The mean age of the patients reached 80.1 years, and 23 (46%) completed all visits. Serum concentrations of total IgG, IgM and IgA increased at all follow-up time points. The ANA fluorescence light intensity units increased at 12 weeks and 12 months postoperatively (p < 0.0001), but the proportion of ANA-positive patients did not change (35%). The values of anti-C1q mildly increased at all follow-up visits, but not the ratio to total IgG. Anti-dsDNA remained negative in all patients, and anti-cardiolipin IgG/IgM antibodies did not change. Anti-CMV IgG antibodies increased significantly at all follow-up visits, without change in the ratio to total IgG. Flow cytometry showed an increased proportion of B-cells 3-4 days postoperatively. In conclusion, major musculoskeletal trauma in elderly patients induces a generalized non-specific increase in immunoglobulin production without laboratory signs for enhanced systemic autoimmunity.

Prevalence and Clinical Associations of Anti-C1q Antibodies in Paediatric Systemic Lupus Erythematosus in Indian Children

Background: Paediatric systemic lupus erythematosus (pSLE) is a heterogeneous, chronic autoimmune disease characterised by multi-system inflammation and the production of antibodies-directed self-antigens. Anti-C1q has been associated with SLE as well as other connective tissue diseases. They have been considered as a marker for disease activity and the presence of nephritis. Objectives: To determine the prevalence of anti-C1q antibodies in the paediatric SLE and to determine clinical associations of elevated anti-C1q antibody levels, especially with lupus nephritis. Methods: All consecutive children with SLE on treatment with immunosuppressive drugs attending our clinic were recruited. After obtaining informed consent, blood samples were tested for anti-C1q antibodies by a commercially available ELISA kit. The prevalence of anti-C1q and its association with lupus nephritis were determined. Results: Out of a total 150 children with SLE, anti-C1q positivity was present in 95 children (64%), at a cut-off value of 20 U/mL. Children with proteinuria, low C3, low C4 and anti-dsDNA positivity had significantly more anti-C1q antibody positivity. Children with lupus nephritis were significantly more likely to have anti-C1q antibody positivity than children without renal involvement (74% vs. 51%, p = .02). Among the children with lupus nephritis, children with active renal disease were more likely to have anti-C1q positivity than in children with quiescent disease (88% vs. 53%, p = .002). Anti-C1q antibodies had a sensitivity of 74% and specificity of 54% at a cut-off value of 22 U/L for renal disease in pSLE. Conclusion: In our study, children with lupus nephritis were significantly associated with elevated anti-C1q antibodies, and children with active renal disease had higher anti-C1q positivity than those with quiescent disease. Anti-C1q levels showed significant associations with low C3, low C4 and anti-dsDNA positivity. Anti-C1q levels did not show significant associations with clinical features of SLE like malar rash, arthritis and CNS involvement. Anti-C1q antibody titres were found to have a positive correlation with renal disease and hence could be used as an adjunctive biomarker in monitoring the disease activity in children with lupus nephritis.

Autoantibodies against Complement Classical Pathway Components C1q, C1r, C1s and C1-Inh in Patients with Lupus Nephritis.

Autoantibodies against the complement component C1q (anti-C1q) are among the main biomarkers in lupus nephritis (LN) known to contribute to renal injury. C1q, the recognition subcomponent of the complement classical pathway, forms a heterotetrameric complex with C1r and C1s, and can also associate a central complement regulator and C1 Inhibitor (C1-Inh). However, the frequency and the pathogenic relevance of anti-C1r, anti-C1s and anti-C1-Inh autoantibodies remain poorly studied in LN. In this paper, we screened for anti-C1q, anti-C1r, anti-C1s and anti-C1-Inh autoantibodies and evaluated their association with disease activity and severity in 74 LN patients followed up for 5 years with a total of 266 plasma samples collected. The presence of anti-C1q, anti-C1r, anti-C1s and anti-C1-Inh was assessed by ELISA. IgG was purified by Protein G from antigen-positive plasma and their binding to purified C1q, C1r and C1s was examined by surface plasmon resonance (SPR). The abilities of anti-C1q, anti-C1r and anti-C1s binding IgG on C1 complex formation were analyzed by ELISA. The screening of LN patients’ plasma revealed 14.9% anti-C1q positivity; only 4.2%, 6.9% and 0% were found to be positive for anti-C1r, anti-C1s and anti-C1-Inh, respectively. Significant correlations were found between anti-C1q and anti-dsDNA, and anti-nuclear antibodies, C3 and C4, respectively. High levels of anti-C1q antibodies were significantly associated with renal histologic lesions and correlated with histological activity index. Patients with the most severe disease (A class according to BILAG Renal score) had higher levels of anti-C1q antibodies. Anti-C1r and anti-C1s antibodies did not correlate with the clinical characteristics of the LN patients, did not interfere with the C1 complex formation, and were not measurable via SPR. In conclusion, the presence of anti-C1q, but not anti-C1s or anti-C1r, autoantibodies contribute to the autoimmune pathology and the severity of LN.

High frequency of concurrent anti-C1q and anti-dsDNA but not anti-C3b antibodies in patients with Lupus Nephritis

ABSTRACT Lupus Nephritis (LN) in patients with Systemic Lupus Erythematosus (SLE) is one of the most serious and prevalent manifestations. The procedure of renal biopsy is harmful and accompanied by potential hazards. Therefore, introducing reliable biomarkers to predict LN is exceedingly worthwhile. In the present study, we compared the diagnostic values of circulating autoantibodies against dsDNA, C1q, C3b, SSA, SSB, and Sm alone or in combination to predict LN. This study evaluated the abovementioned autoantibodies in 40 healthy controls (HCs) and 95 SLE patients with different kidney involvements, including absent (n = 40), inactive (n = 20), and active (n = 35) LN using EIA method. The frequency and odds ratio of anti-dsDNA (71.4%, OR = 4.2), anti-C1q (62.9%, OR = 5.1), and the simultaneous existence of anti-C1q and anti-dsDNA (51.4%, OR = 6) antibodies were significantly higher in the active LN group compared with both inactive and absent LN groups. Moreover, the levels of anti-C1q and anti-dsDNA antibodies positively correlated with disease activity in patients with SLE. The prevalence of these autoantibodies was associated with the severity of LN biopsies. These data suggest that anti-C1q and anti-dsDNA antibodies and also their simultaneous presence may be valuable diagnostic biomarkers for LN prediction in patients with SLE.

Complements as a Predictive Biomarker of Lupus Nephritis in Female Patients with Systemic Lupus Erythematosus

Background: Lupus nephritis (LN) has been demonstrated in about 40–50 percent of all systemic lupus erythematosus (SLE) patients. Patients having renal flares are at risk from suffering serious kidney damage, and usually have a poor prognosis. Unfortunately, renal flare pathogenesis in LN patients remains unclear, and no known predictions of an impending renal flare exist. Aim: The present study aims to measure circulating levels of anti-C1q antibodies, C3, C4, TNF-α and soluble TNF-α receptor, serum creatinine and blood urea nitrogen (BUN) as biomarkers for active LN. Materials and methods: The study included 180 SLE female patients meeting the revised classification requirements of the modified American College of Rheumatology (ACR); 90 female patients with active proliferative LN (biopsy-proven) and other 90 patients with inactive LN. Patients were receiving mycophenolate mofetil; and the study was conducted between 2018 and 2019. Results: We found that low levels of complement C3 and C4 in combination with high levels of BUN, creatinine, anti-C1q antibodies and positive anti-dsDNA antibodies were more likely to be associated with lupus nephritis development in SLE patients. Also, high levels of TNF-α and its soluble receptor can be used as an indication of active disease activity and flare development. Conclusion: Monitoring of Anti-C1q antibodies, C3, C4, serum creatinine, and BUN levels in SLE patients can improve LN prognosis. TNF-α can also be used as an indicator for active LN and concomitant flare. This early diagnosis combined with prompt care would help decrease morbidity and mortality in LN patients.

Correlation of Serum Anti-Clq Antibody Levels and Disease Activity in Patients with Systemic Lupus Erythematosus

Background. Antibody to complement C1q (Anti-C1q Antibody) can be found in Systemic Lupus Erythematosus (SLE) patients. Complement C1q plays a role in the clearance of apoptotic cells and immune complexes. Anti-C1q causes complement C1q become inactive so that the clearance decreases, which induces self antigen and inflammatory response. Many tissue inflammation are associated with disease activity and lupus manifestations. The aim of this study is to find out the correlation of anti-C1q level with disease activity, so that anti-C1q can be used as an objective indicator of inflammation along with SELENA-SLEDAI. &#x0D; Method. This is an analytic descriptive study with cross sectional design. Anti-C1q antibody levels were measured in 52 SLE patients who are hospitalized or treated routinely in outpatient clinic of Rheumatology Dr.Hasan Sadikin Hospital Bandung Indonesia from October to December 2015.&#x0D; Result. Most of the study subjects were women (94%), with a median age of 33 years. There were 13 new patients (25%), and the rest 42 patients were treated routinely. The median SELENA-SLEDAI was 6 (0-32). Subject were divided into no activity (11.5%), low disease activity (34.6%), medium disease activity (25%) high disease activity (15.4%) and very high disease activity (13.5%). Median anti-C1q level was 3.92 U/mL (range 0.6-100.2 U/mL). Anti-C1q antibody levels were positively correlated with SLE disease activity based on SELENA-SLEDAI scores (r=+0.304; p=0.014)&#x0D; Conclusion. Anti-C1q antibody levels has mild correlated with lupus disease activity based on SELENA-SLEDAI score&#x0D; Keywords : Anti-C1q antibody, SLE, SELENA-SLEDAI.

SERPINB3 Delays Glomerulonephritis and Attenuates the Lupus-Like Disease in Lupus Murine Models by Inducing a More Tolerogenic Immune Phenotype.

Objective: To explore the effects of SERPINB3 administration in murine lupus models with a focus on lupus-like nephritis.Methods: 40 NZB/W F1 mice were subdivided into 4 groups and intraperitoneally injected with recombinant SERPINB3 (7.5 μg/0.1 mL or 15 μg/0.1 mL) or PBS (0.1 mL) before (group 1 and 2) or after (group 3 and 4) the development of proteinuria (≥100 mg/dl). Two additional mice groups were provided by including 20 MRL/lpr mice which were prophylactically injected with SERPINB3 (10 mice, group 5) or PBS (10 mice, group 6). Time of occurrence and levels of anti-dsDNA and anti-C1q antibodies, proteinuria and serum creatinine, overall- and proteinuria-free survival were assessed in mice followed up to natural death. Histological analysis was performed in kidneys of both lupus models. The Th17:Treg cell ratio was assessed by flow-cytometry in splenocytes of treated and untreated MRL/lpr mice. Statistical analysis was performed using non parametric tests and Kaplan-Meier curves, when indicated.Results: Autoantibody levels and proteinuria were significantly decreased and time of occurrence significantly delayed in SERPINB3-treated mice vs. controls. In agreement with these findings, proteinuria-free and overall survival were significantly improved in SERPINB3-treated groups vs. controls. Histological analysis demonstrated a lower prevalence of severe tubular lesions in kidneys of group 5 vs. group 6. SERPINB3-treated mice showed an overall trend toward a reduced prevalence of severe lesions in both strains. Th17:Treg ratio was significantly decreased in splenocytes of MRL/lpr mice treated with SERPINB3, compared to untreated control mice.Conclusions: SERPINB3 significantly improves disease course and delays the onset of severe glomerulonephritis in lupus-prone mice, possibly inducing a more tolerogenic immune phenotype.

Multiplex immunoassay detection of autoimmune disease autoantibodies in serum and plasma

Abstract Autoantibody formation is principal to the pathogenesis of a variety of autoimmune diseases. Dysregulated apoptosis and the subsequent defective clearance of cellular debris leads to the exposure of autoantigens and the generation of autoantibodies. The presence of autoantibodies may indicate disease activity, prognosis, and clinical associations related to a variety of autoimmune diseases, including systemic lupus erythematosus (SLE), Sjögren’s Syndrome, Scleroderma, Polymyositis/Dermatomyositis, and various overlap syndromes of these diseases. Here we report the development of a multiplex immunoassay to monitor 20 autoantibodies present in blood that are involved in a variety of autoimmune diseases: SSA/Ro60, SSA/Ro52, SSB/La, RNP, RNP/Sm, Sm, Ribosomal P, Proteinase 3, Myeloperoxidase, PCNA, β 2-Glycoprotein, CENP-A, CENP-B, Scl-70, Jo-1, C1q, PM/Scl-100, Ku, Mi-2, and PL-12. Using the 20-plex immunoassay, we measured expression of autoantibodies in serum and plasma from SLE patients with various disease manifestations and overlap syndromes, healthy controls, and CDC reference samples available for 11 autoantibodies. Additionally, control beads were included in the immunoassay. Levels of SSA/Ro60, SSA/Ro52, SSB/La, RNP, RNP/Sm, and Sm matched clinical laboratory features noted at the time of SLE sample collection. Additionally, anti-C1q antibody levels were associated with lupus nephritis. The CDC controls exhibited elevated MFI for the autoantibodies for which they were expected to react strongly. This study demonstrates the value of using multiplex technology to evaluate multiple autoantibodies, allowing for an extensive autoantibody profile to evaluate patients with various autoimmune diseases.

Predisposition of IL-1β (-511 C/T) polymorphism to renal and hematologic disorders in Indian SLE patients

ObjectiveTo see the role of IL-1β gene polymorphisms to disease susceptibility in Indian SLE patients. Materials and methodsThis case-control study included 200 SLE patients and 201 controls. Serum levels of IL-1β and anti-C1q antibodies were measured by multiplex immunoassay and ELISA respectively. Genotyping of SNPs in IL-1β (-511C/T and +3954C/T) were performed by PCR-RFLP method. Autoantibody profile was done in 141 SLE patients. ResultsMean serum levels of IL-1Β were significantly higher (10.9±5.3pg/ml) in patients compared to controls (7.0±2.0pg/ml) (p<0.0001). Similarly, mean levels of IL-1β were significantly elevated among patients with renal and hematologic manifestations. IL-1Β levels were negatively correlated with hemoglobin concentration (r=−0.25, p=0.001). A statistically significant difference was observed for IL-1β -511CC genotypes (OR=2.9, p=0.0068, Pc=0.0136) in patients with Lupus Nephritis (LN) as compared to SLE patients without nephritis. The IL-1β+3954CT genotype (OR=2.0, p=0.0032, Pc=0.0064) and +3954T allele (OR=1.9, p=0.0017, Pc=0.0034) showed significantly higher frequency among patients as compared to controls. Furthermore, the -511C allele showed higher prevalence in patients with renal (OR=1.6, p=0.0335) and hematologic (OR=1.6, p=0.0326) manifestations among SLE patients. ConclusionIL-1β gene polymorphisms appear to confer susceptibility to the disease in Indian SLE patients.

Diminished capacity of opsonization and immune complex solubilization, and detection of anti-C1q antibodies in sera from patients with hereditary angioedema

BackgroundHereditary angioedema (HAE) is an autosomal dominant disease caused by deficiency of C1 esterase inhibitor. Symptoms of HAE include edema, which can potentially cause suffocation. Some patients with HAE exhibit immunological abnormalities, which could prevent an accurate diagnosis. Low levels of complement components are characteristic of HAE and in other settings are thought to reduce elimination of apoptotic cells and immune complex (IC). Thus, we aimed to experimentally clarify the mechanism of immunological abnormalities using sera from HAE patients. MethodsSerum samples from 18 patients with HAE were collected when free from angioedema attack and compared with normal human pooled sera (NHPS) from 20 healthy volunteers. Opsonization was measured as the rate of phagocytosis of apoptotic Jurkat cells by macrophages differentiated from THP-1 cells incubated with serum. IC solubilization in serum was analyzed by quantifying peroxidase released from a synthetic IC composed of peroxidase and anti-peroxidase antibodies. Anti-C1q antibody levels were detected using an enzyme-linked immunosorbent assay. ResultsSerological immunological abnormalities were detected in 12 patients. Opsonization in serum samples from each patient with HAE was lower than that in NHPS (∼20% versus 70%, respectively). The rate of IC solubilization was lower in serum from HAE patients than NHPS. Some patients had high serum anti-C1q antibody levels with increased serum IC levels. ConclusionsSera from patients with HAE exhibit anti-C1q antibodies, with a lower capacity for opsonization and IC solubilization. This may be associated with immunological abnormalities and should be investigated further to facilitate accurate diagnosis of HAE.

Anti-C1q autoantibodies are linked to autoimmune thyroid disorders in pregnant women.

Anti-C1q antibodies (anti-C1q) have been implicated in the pathogenesis of autoimmune diseases, including autoimmune thyroid disorders (AITD). The aim of this study was to evaluate the association between anti-C1q and thyroid function in pregnancy-associated AITD. In 96 pregnant women screened positive for AITD (thyroid dysfunction and/or antibodies against thyroperoxidase - TPOAb), anti-C1q were measured during the 9-11th gestational week and after delivery (median 16 months after delivery), and compared to the corresponding serum levels of thyroid hormones. As controls, 80 healthy pregnant women, 72 non-pregnant AITD patients and 72 blood donors were included. In the non-pregnant AITD group, two serum samples ≥6 months apart were analysed. Compared to blood donors, anti-C1q levels were substantially higher in all pregnant women analysed. In pregnancy, anti-C1q levels were higher in the TPOAb-positive women than in controls (37 versus 17·5%, P<0·0001). Anti-C1q-positive pregnant women screened positive for AITD had higher thyroid-stimulating hormone (TSH) levels than anti-C1q-negative women (2·41 versus 1·94 mU/l, P=0·01), and TSH correlated positively with anti-C1q (r=0·226, P=0·045) in the TPOAb-positive women. After delivery, serum levels of anti-C1q decreased in the positively screened TPOAb-negative women (8·8 versus 5·9 U/l, P=0·002), but not in the TPOAb-positive ones, and they no longer correlated with TSH. Anti-C1q antibody levels increase during pregnancy in general and even more in the context of AITD, where they correlate with thyroid stimulating hormone levels.

Autoantibodies against a complement component 1 q subcomponent contribute to complement activation and recurrent thrombosis/pregnancy morbidity in anti-phospholipid syndrome.

To investigate the prevalence and significance of the autoantibodies against complement component 1 q subcomponent (C1q) in patients with APS. In all, 40 consecutive primary APS patients, 42 patients with non-SLE CTDs and 20 SLE patients negative for aPL were enrolled in this retrospective analysis. Refractory APS was defined as a clinical status of recurring thrombosis or pregnancy morbidity during adequate secondary prophylaxis. An ELISA was used to measure serum levels of anti-C1q antibodies and anaphylatoxins (C3a, C4a). Anti-C1q antibodies were found in 36% (15/42) and 2.5% (1/40) of primary APS patients and controls, respectively. Among primary APS patients, anti-C1q antibody titres were significantly correlated with serum C4a levels (P = 0.013). Neither the prevalence nor the titre of anti-C1q antibodies was associated with any specific clinical manifestations of APS, nor titres of aPL. Refractory APS patients (n = 10) had a higher prevalence of anti-C1q antibodies (9/10 vs 6/32, P = 0.01) than APS patients without recurrence (n = 32). Anti-C1q antibodies are associated with complement activation in APS and may contribute to the pathogenesis, particularly in refractory cases.

Correlation of Serum Soluble Interleukin-7 Receptor and Anti-C1q Antibody in Patients with Systemic Lupus Erythematosus.

Background. Serum concentrations of soluble interleukin-7 receptor (sIL-7R) and anti-C1q antibody have recently been identified as unique serological markers for lupus nephritis (LN) in patients with systemic lupus erythematosus (SLE). In this study, we evaluated the correlation of serum sIL-7R and anti-C1q in SLE patients. Methods. Sera from 134 patients with SLE and 84 healthy cohorts were tested for levels of sIL-7R and anti-C1q antibodies in terms of ELISA. Correlations of the sIL-7R and anti-C1q autoantibodies were evaluated. Results. The serum concentrations of sIL-7R and anti-C1q antibodies were significantly higher in SLE patients and LN patients in comparison with healthy individuals/controls and SLE patients with non-LN, respectively. In addition, both sIL-7R and anti-C1q concentrations were found to significantly correlate with the SLE disease activity as evaluated by SLEDAI scores. Interestingly, the serum sIL-7R concentration was strongly correlated with the level of anti-C1q antibodies (r = 0.2871, p = 0.0008) but not statistically correlated with other serological markers, including the anti-dsDNA and complements C3 and C4 concentrations in SLE patients. Conclusion. Both serum sIL-7R and anti-C1q antibodies were strongly associated with disease activity and LN in SLE patients, suggesting that they may be reliable serological markers for identification of SLE patients with active diseases and LN.

Effect of Rituximab on Serum Levels of Anti-C1q Antibodies and Antineutrophil Cytoplasmic Autoantibodies in Refractory Severe Lupus Nephritis

Effect of Rituximab on Serum Levels of Anti-C1q Antibodies and Antineutrophil Cytoplasmic Autoantibodies in Refractory Severe Lupus Nephritis

PTX3, Anti-PTX3, and Anti-C1q Autoantibodies in Lupus Glomerulonephritis.

Pentraxin 3 (PTX3) is an acute-phase protein involved in C1q clearance. The presence of anti-C1q and the absence of anti-PTX3 antibodies were associated with lupus glomerulonephritis (LGLN). Our aim was to assess soluble and kidney-expressed PTX3 and their relationships with anti-C1q and anti-PTX3 antibodies in LGLN. Serum PTX3, anti-C1q, anti-dsDNA, and anti-PTX3 antibodies were tested in 130 systemic lupus erythematosus (SLE) patients, 130 healthy and 127 disease controls. Twenty-nine renal biopsies from SLE patients were analyzed and PTX3 immunostaining was quantified by morphometric analysis. Parametric and nonparametric statistics were performed. PTX3 serum levels were lower in SLE versus controls, but they were correlated with proteinuria in LGLN patients (p = 0.001). LGLN patients had higher anti-C1q and lower anti-PTX3 antibody levels than those without (p < 0.0001). LGLN was more prevalent in anti-C1q(+)/anti-PTX3(-) than in anti-C1q(+)/anti-PTX3(+) patients (p < 0.001). No LGLN was observed in anti-C1q(-)/anti-PTX3(+) patients. PTX3 was expressed in glomeruli and renal interstitium. Renal PTX3 was correlated with proteinuria (p = 0.024) and interstitial fibrosis (p = 0.023). PTX3 staining and fibrosis were higher in anti-PTX3(-) than anti-PTX3(+) patients. In conclusion, PTX3 is expressed in glomeruli of LGLN patients, primarily in anti-PTX3(-) patients, where it is correlated with renal fibrosis. Anti-C1q/anti-PTX3 antibody profile seems to be useful in LGLN assessment.

Anti-C1q Antibody as a Predictor of Chronic HCV Genotype 4 Response to Treatment in Egyptian Children

Background: Hepatitis C virus (HCV) infection has been reported to be the most common blood born pathogen all over the world. The prevalence of HCV in children in developed countries ranges between 0.1 and 0.4 %, and is generally lower than in adults. Combinedpegylated interferon and ribavirin is still the only standard of care treatment in spite of its side effects, high costs and low sustained virological response (SVR) rates. Hence, this provides a compelling reason for the identification of biomarker predictors of disease response to treatment. Objective: To evaluate anti-C1q antibody as a predictor of chronic HCV response to treatment with combined pegylated interferon alpha-2b and ribavirin in Egyptian children. Methodology: This study was conducted on forty-four chronic HCV-infected children (Male/Female: 30/14; aged 12.02±3.1 years) from the outpatient clinic, Pediatric Hepatology Department, National Liver Institute, Menoufiya University. They were given combined pegylated interferon alpha-2b (Peg-IFN-α-2b) and ribavirin (RBV) for 48 weeks and a quantitative polymerase chain reaction (PCR) for hepatitis C virus Ribonucleic acid was performed at 12, 24, 48 weeks during treatment and after another 24 weeks post-treatment. Anti-HCV antibody and Real-time PCR for HCV-RNA was performed (the detection limit was 15 IU/mL). Anti-C1q antibodies were performed by enzyme-linked immunosorbent assay (ELISA). Results: Serum levels of Anti-C1q antibodies were significantly higher (P = 0.001) in the Non-responders group (mean = 14.61± 6.749ng/ml) compared to the SVR one (mean = 2.27 ± 3.77ng/ml). No statistically significant difference (P > 0.05) had been found between SVR and Non-responders regarding the age, ALT, viral load, or hepatic necroinflammatory activity and liver fibrosis. Anti-C1q at a cutoff value of9.05ng/ml, had sensitivity and specificity of 84.6% and 75% respectively and 92% positive predictive value. No significant correlation between the serum level of anti-C1q antibodies and the age, sex or HCV viral load, liver enzymes, and the degree of fibrosis and necroinflammatory activity was found (P> 0.05) for all parameters. Conclusion: Anti-C1q could be a good predictor for HCV treatment and should be included in pretreatment laboratory assessment for proper choice of chronic HCV children patients who will benefit from combination therapy.

Effect of Rituximab on Serum Levels of Anti-C1q and Antineutrophil Cytoplasmic Autoantibodies in Refractory Severe Lupus Nephritis.

The objective of this study was to analyze and compare the effects of rituximab (RTX) and cyclophosphamide (CTX) on the serum levels of anti-C1q antibodies and antineutrophil cytoplasmic autoantibodies (ANCA) in assessing the prognosis of severe and refractory lupus nephritis (LN). Eighty-four cases of severe and refractory LN were randomly divided into two groups of 42 cases each: CTX group and RTX group (CTX+RTX) during February 2010 to February 2014 in our hospital. Changes in serum levels of anti-C1q antibodies and ANCA in the two groups were examined, and efficacies of the drugs were compared. The total efficacy of RTX group was found to be 83.3 %, which was significantly higher than that of the CTX group, 57.1 % (p < 0.05). The serum anti-C1q antibodies and ANCA were decreased to 11.9 and 26.2 % in the RTX-treated group, which was significantly lower than those observed in the CTX-treated patients (21.4 and 69.0 % respectively) (p < 0.05). The clinical indices of LN were significantly improved in the two groups after the treatment. However, the urinary protein, albumin, complement C3, the percentage of CD19(+)B cells, and SLEDAI scores in the RTX group were significantly lower than those in the CTX group (p < 0.05). RTX plus with CTX showed a better therapeutic efficacy compared to CTX, and it significantly improved the prognosis of refractory and severe LN. The improvement in disease prognosis was directly related to the reduced serum levels of anti-C1q and ANCA measured during the course of treatment suggesting that they can serve to be valuable biomarkers of LN prognosis. Moreover, the measurement can assist in the judgment of RTX efficacy guiding the adjustment of the drug dose to improve the quality of life.

The Usefulness of Endothelial Cell Adhesion Molecules and Anti-C1q Antibody in Monitoring Systemic Lupus Erythematosus Disease Activity.

Objectives. The study was conducted to determine the correlation of ICAM-1, VCAM-1, and anti-C1q antibody levels with SLE disease activity index (SLEDAI) and standard SLE disease activity immunological markers (anti-dsDNA and sera C3 and C4). Study Design. This was a cross-sectional study. Materials and Methods. Blood samples were obtained from 95 SLE patients (45 active SLE and 50 nonactive SLE) and 50 controls. The subjects were assessed using SLEDAI and score of more than five is determined as having active SLE. The sera were tested for serum ICAM-1, VCAM-1, and anti-C1q (ELISA), anti-dsDNA (CLIFT), serum C3, and serum C4 (immunonephelometry). Results. Anti-dsDNA and anti-C1q antibody showed good positive correlations with SLEDAI (r = 0.529, P < 0.001 and r = 0.559, P < 0.001, resp.). VCAM-1 and sera C3 and C4 showed fair correlation with SLEDAI (r = 0.294, P = 0.004; r = −0.312, P = 0.002; and r = −0.382, P < 0.001, resp.). ICAM-1 level showed no significant correlation with SLEDAI (P = 0.062). There were significant correlations of VCAM-1 and anti-C1q antibody with anti-dsDNA (r = 0.226, P = 0.006 and r = 0.511, P < 0.001, resp.). VCAM-1 showed poor inverse correlation with serum C3 (r = −0.183, P = 0.028) and fair inverse correlation with serum C4 (r = −0.251, P = 0.002). Anti-C1q antibody demonstrated fair inverse correlation with both sera C3 and C4 (r = −0.420, P ≤ 0.001 and r = −0.398, P < 0.001, resp.). However, ICAM-1 showed no significant correlation with anti-dsDNA and sera C3 and C4 (P = 0.259, P = 0.626 and P = 0.338, resp.). Conclusions. The serum levels of anti-C1q antibody in SLE patients showed the best correlation with the SLEDAI and standard immunological tests for SLE disease activity. These data support that anti-C1q antibody is a useful marker for monitoring SLE global disease activity. The potential of VCAM-1 needs further confirmation.

Complement activation in patients with neuromyelitis optica

The role of complement has been demonstrated in experimental models of neuromyelitis optica (NMO), however, only few studies have analysed complement components longitudinally in NMO patients. We measured serum or plasma concentrations of anti-C1q antibodies and complement split products C3a and C4a and soluble C5b-9 in patients with NMO, multiple sclerosis and healthy controls. NMO patients had higher levels of C3a and anti-C1q antibodies than healthy controls. C3a levels correlated with disease activity, neurological disability and aquaporin-4 IgG in NMO patients suggesting a role of the alternative pathway of complement in the pathogenesis of NMO and supporting the strategy of therapeutic complement inhibition.

AB0692 Anti-C1Q antibodies in correlation with lupus nephritis in patients treated by rituximab

ObjectivesThe aim of the study was to assess the levels of the antibody to C1q complement component (anti-C1q) in the sera of patients (pts) with lupus nephritis (LN) in relation...