Intended Use
Anti-C1q is an indirect solid phase enzyme immunoassay (ELISA) for the determination of IgG class autoantibodies against C1q in human serum or plasma. The assay is intended for research use only, not for use in diagnostic procedures.
Storage
The microtiter well plate and all other reagents are stable at 2-8°C until the expiration date printed on the label. The whole kit stability is usually 12 months from the date of shipping under appropriate storage conditions. Do not contaminate the bottles. Withdraw solutions in a separate clean tube or dispensing trays. Any unused solution should be discarded and not returned to the bottle. Do not use HRP substrate solution if this solution is blue. Do not expose these solutions to strong light.
Precision
Statistics for coefficients of variation (CV) were calculated for each of three samples from the results of 24 determinations in a single run for Intra-Assay precision. Run-to-run precision was calculated for each of 3 samples from the results of 16 determinations in two runs.
Intra-Assay
Mean 25.2, 58.6, and 75.4 with 3.7%, 2.9% and 2.8% CV respectively.
Intra-Assay
Mean 22.2, 33.6, and 53.4 with 4.7%, 2.5% and 1.9% CV respectively.
Sensitivity
The lower detection limit for the Anti-C1q test was determined at 0.5 U/ml.
The highest Anti-C1q titers were found in patients with active lupus nephritis. It was also demonstrated that rises in Anti-C1q titers have predictive value for ensuing relapses of lupus nephritis. It is described that in some cases patients with clinical active lupus were found as Anti-ds DNA negative, so Anti-C1q antibodies may serve as an additional tool for rheumatologist to document lupus activity.
General Description
The complement system, a central component of innate immunity, exhibits three pathways of activation classical, alternative, and lectin-mediated. C1, a key component of the classical pathway, is actually a complex of three proteins C1q, C1r, and C1s. C1q is serum glycoprotein of 18-polypeptides chains consisting of three non-identical subunits, A (29 kDa), B (26 kDa), and C (246 aa, 19 kDa) in molar ratio of 1:2:2. C1Q in the plasma is complexed with two proenzymes C1r and two C1s molecule to form the first component of complement (C1). Activation of complement via classical pathway is triggered by binding of globular head of C1q to immune complexes containing IgG (Fc-region) or IgM or to a variety of other activating substances, including C-reactive protein, retrovirus, and mitochondria. Subsequent to C1q binding, c1r and C1s are converted to proteolytic enzymes that are responsible to continuation of activation via the classical pathway.
Alternatively, high-affinity autoantibodies directly recognize the collagenous "tail" portion of C1q through the antibody F(ab) antigen- combining sites rather than via the Fc domain. Anti-C1q autoantibodies have been commonly identified in patients with autoimmune diseases such as systemic lupus erythematosus (SLE) and hypocomplementemic urticarial vasculitis. Anti-C1q antibodies preferentially localized in the glomeruli of patients with SLE. Lupus nephritis (LN), the renal disease that accompanies SLE. Anti-C1q autoantibodies have been suggested to be closely associated with LN. Conversely, in the absence of antiC1q autoantibodies, no LN develops. Serial measurement of Anti-C1q titers will be an effective tool for the guidance of immunosuppressive therapy in SLE patients. Anti-C1q autoantibodies may be especially relevant for monitoring of lupus nephritis activity.
Citations
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