Anti-C1Q Antibodies Concentrations by Elisa in Systemic Lupus Erythematosus

Abstract

Systemic lupus erythematosus (SLE) is an inflammatory disorder in which autoantibodies contribute to impaired apoptosis and clearance of cell debris. Anti dsDNA and anti C1q antibodies have been implicated, as well as complement protein C1q itself. IgG autoantibodies reacting with the collagen-like region of C1q protein (αC1q ab) were quantitated in serum of 56 patients diagnosed with SLE and undergoing treatment for variable periods, together with 33 age/sex-matched controls. Analysis of the results showed optimal sensitivity and specificity of 57% and 91% respectively at a cut-off concentration for positivity of 20 U/ml. The assay is a potentially useful confirmatory test for SLE, but is not suitable as a screening test for SLE with the probability of a positive test and SLE in an individual within a random population of only ≤ 1%. αC1q ab concentrations were detectable in all samples tested with concentrations manifesting no correlation with age and serum C1q levels in SLE patients and a negative correlation with age in controls. The αC1q ab detected by this assay do not react therefore with native C1q. In SLE patients, αC1q ab concentrations correlated with the concentrations of dsDNA antibodies, (p=0.0001) and Creactive protein and inversely with complement component C4 (C4) concentrations (p=0.041). αC1q ab concentrations were not associated with individual therapeutic regimens, but were higher in those patients receiving a combination of three drug therapies and with the presence of renal disease. The diagnostic relevance of this complex autoantibody will require further definition of its antigenic specificities. Lupus

Insights on the relationship between complement component C4 serum concentrations and C4 gene copy numbers in a Western Australian systemic lupus erythematosus cohort

“…We have previously reported the assay methods used to measure C4 concentrations in the serum of the SLE and control cohorts. 15…”

“…These are summarized in a previous publication. 15 SLE patients in this cohort were treated with various therapeutic regimens including steroids (low-dose prednisolone 5 mg/day), steroid-sparing immunosuppressant therapies (azathioprine, cyclosporine, cyclophosphamide, methotrexate, mycophenolate mofetil) and antimalarial therapy (hydroxychloroquine). Thirty-three age and sex-matched healthy control subjects (47 AE 15 years) (mean AE SD) were recruited from the Perth metropolitan area.…”

“…We have previously reported the assay methods used to measure C4 concentrations in the serum of the SLE and control cohorts. 15 Determination of complement C4, C4A and C4B gene copy number, HERV-K retroviral element in intron 9 and CT insertion in exon 29 of the C4 genes The C4 GCN was assessed using Taqman TM realtime PCR methodology, which has been previously described elsewhere. 14 The presence of the HERV-K retroviral element in intron nine of the C4 genes was assessed by real-time PCR on a VIIA 7 thermocycler (ThermoFisher Scientific) using Taqman TM (Life Technologies) custom copy number assay designed from published primers (C4L: C4Fin95 5'-TTGCTCGTTCTGCTCATTC CTT-3' and C4L-3LTR-R 5'-GTTGAGGCTGG TCCCCAACA-3'; C4S: C4Fin95 5'-TTGCTCGT TCTGCTCATTCCTT-3' and C4Sin9R-2 5'GGC GCAGGCTGCTGTATT-3') and probe (C4in95 FAM/MGB -5'-CTCCTCCAGTGGACATG-3').…”