C1q ELISA Kit [Mouse], 2 x 96 det. (CAT#: CB-P100-K) Datasheet

Kit

C1q, together with C1r and C1s, form the first part of the classical complement pathway, the C1 macromolecule. 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 complexes with these immune systems. When the antibodies in the body are docked, 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. As long as the immunoglobulin and IgG or The heavy chain of IgM can play the role of the recognition unit, provided that the immunoglobulin binds to the antigen, C1q can bind to the apoptotic globules, thereby activating the classical complement pathway and mediating phagocytosis. Therefore, C1q promotes the development of apoptotic cells. Elimination and subsequent exposure of self-antigens, thereby preventing the stimulation of t1. His immune system. C1q is mainly produced by macrophages, but also by follicular dendritic cells, finger cells and cells of the monocyte-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 cause autoimmunity by impairing the clearance of apoptotic cells. Anti-C1q autoantibodies are deposited together with C1q in the glomerulus, 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 of the C1QA gene leads to a decrease in C1q serum levels, and is related to the specific skin disease of photosensitive lupus, subacute cutaneous lupus erythematosus (SCLE).

Mouse C1q ELISA kit is used to quantitatively determine mouse C1q in serum and plasma samples in vitro.

Mouse 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 form of the plate with twelve disposable 8-well plates allows free choice of batch size for determination. Samples and standards are incubated in microtiter wells coated with antibodies that recognize mouse C1q. The biotinylated tracer antibody will bind to the captured mouse 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 mouse C1q standard. The concentration of the mouse C1q sample running simultaneously with the standard can be determined from the standard curve.