QuickStep Human IgA (Immunoglobulin A) ELISA Kit

This ELISA kit uses the Sandwich-ELISA principle. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to Human IgA. Samples (or Standards) and biotinylated detection antibody specific for Human IgA are added to the micro ELISA plate wells. Human IgA would combine with the specific antibody. Then Avidin-Horseradish Peroxidase (HRP) conjugate are added successively to each micro plate well and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain Human IgA, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of stop solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 ± 2 nm. The OD value is proportional to the concentration of Human IgA. You can calculate the concentration of Human IgA in the samples by comparing the OD of the samples to the standard curve.

First described in serum in 1953, IgA is the second dominant isotype in the blood circulation following IgG. It can be found in both monomeric and polymeric forms. Circulating IgA is in monomeric form, whereas secretory IgA, in the mucosal secretions of respiratory, intestinal, and genitourinary systems, is dimeric. In humans, there are two subclasses of IgA: IgA1 and IgA2, constant heavy chains of which are encoded by two separate α1 and α2 genes on chromosome 14 [1]. The main structural difference between them is that IgA2 has a shorter hinge region which may render this isotype more resistant to bacterial proteases in the lumen of gastrointestinal or respiratory systems. In the blood, IgA interacts with an Fc receptor called FcαRⅠ(or CD89), which is expressed on immune effector cells, to initiate inflammatory reactions[2]. Ligation of FcαRⅠ by IgA containing immune complexes causes antibody-dependent cell-mediated cytotoxicity (ADCC), degranulation of eosinophils and basophils, phagocytosis by monocytes, macrophages, and neutrophils, and triggering of respiratory burst activity by polymorphonuclear leukocytes. IgA nephropathy is caused by IgA deposits in the kidneys, it is not yet known why IgA deposits occur in this chronic disease. Some theories suggest an abnormality of the immune system results in these deposits.