C1q ELISA Kit [Human], 1 x 96 det. (CAT#: CB-P103-K) Datasheet

Kit

C1q together with C1r and C1s form the first part of the classical complement pathway, C1 macromolecules. The formation of antibody-antigen complexes (immune complexes) is the main way to activate the classical pathway of the complement system. C1q triggers the activation process when it docks on the antibodies in these immune complexes. In this way, C1q acts as a bridge between the innate and adaptive immune systems. The interaction between the immune complex and C1q induces conformational changes in the C1 complex, thereby activating the classical pathway. C1q acts as a recognition unit by binding to the heavy chain of IgG or IgM (Fcγ and Fc micro), provided that the immunoglobulin binds to its antigen. In addition, C1q can bind to apoptotic vesicles, in which it activates the classical complement pathway and mediates phagocytosis. In this way, C1q promotes the clearance of apoptotic cells and subsequent exposure of self-antigens, thereby preventing stimulation of the immune system. C1q is mainly produced by macrophages, but also by follicular dendritic cells, finger cells and cells of the mononuclear macrophage lineage. C1q deficiency has a profound impact on host defense and immune complex clearance. Hereditary C1q deficiency is also associated with the development of systemic lupus erythematosus (SLE). In the absence of C1q, SLE was found in 90% of the reported cases. C1q plays a role in preventing autoimmunity by promoting physiological clearance and processing of apoptotic fragments. Lack of C1q may lead to impaired clearance rate of apoptotic cells, leading to autoimmunity. Anti-C1q autoantibodies are deposited in the glomerulus together with C1q, but only in the case of glomerular immune complex disease can it induce obvious kidney disease. This provides an explanation why anti-C1q antibodies are particularly pathogenic in SLE patients. Low C1q levels are associated with proliferative glomerulonephritis (WHO grade III and IV). In addition, the concentration of C1q will decrease before the clinical manifestations of the disease onset. Low C1q levels have also been shown to predict histopathological results in lupus nephritis. The single nucleotide polymorphism in the C1QA gene leads to a decrease in C1q serum levels, and is associated with the specific skin disease of photosensitive lupus, subacute cutaneous lupus erythematosus (SCLE).

The human C1q ELISA kit is used for the in vitro quantitative determination of human C1q and Ig in serum, plasma and bronchoalveolar lavage fluid (BALF) samples, which contain circulating immune complex (CIC).

Human C1q ELISA kit is a ready-to-use solid-phase enzyme-linked immunosorbent assay based on the sandwich principle. The working time is 3 hours. The effective format of two plates with twelve disposable 8-well strips allows free choice of batch size for determination. Samples and standards are incubated in microtiter wells containing antibodies that recognize human C1q. The biotinylated tracer antibody will bind to the captured human Clq. The streptavidin-peroxidase conjugate will bind the biotinylated tracer antibody. The streptavidin-peroxidase conjugate will react with the substrate tetramethylbenzidine (TMB). The enzyme reaction is stopped by adding oxalic acid. Measure the absorbance at 450nm with a spectrophotometer. Draw a standard curve by plotting the absorbance (linear) relative to the corresponding concentration (logarithm) of the human C1q standard. The human C1q concentration of samples run at the same time as the standard can be determined from the standard curve.