CD357 (AITR/GITR) Monoclonal Antibody (DTA-1), Functional Grade, eBioscience™, Invitrogen™

Beschreibung

Description: The DTA-1 monoclonal antibody reacts with mouse GITR, Glucocorticoid-Induced TNFR family gene, also known as TNFRSF18. In naive mice, GITR is expressed predomitly by CD4+CD25+ T regulatory cells (Treg) and by CD25+ CD4+ CD8- thymocytes. Stimulation of GITR with DTA-1 antibody abrogates Treg cell-mediated suppression. Although it does not deplete CD357 expressing cells in vivo, it has been shown to induce tumorogenesis. The removal of GITR-expressing Treg cells or the administration of DTA-1 resulted in organ specific autoimmune disease. Applications Reported: This DTA-1 antibody has been reported for use in flow cytometric analysis and immunohistochemistry of frozen mouse tissue. It has also been reported for use in functional assays. Applications Tested: This DTA-1 antibody has been tested by flow cytometric analysis of mouse splenocytes. This can be used at less than or equal to 0.03 μg per test. A test is defined as the amount (μg) of antibody that will stain a cell sample in a final volume of 100 μL. Cell number should be determined empirically but can range from 10^5 to 10^8 cells/test. This DTA-1 antibody has been tested by immunohistochemistry of frozen tissue and can be used at less than or equal to 10 μg/mL. It is recommended that the antibody be carefully titrated for optimal performance in the assay of interest. Endotoxin: Less than 0.001 ng/ug antibody as determined by the LAL assay.

Storage and handling: Use in a sterile environment. Filtration: 0.2 μm post-manufacturing filtered. Purity: Greater than 90%, as determined by SDS-PAGE. Endotoxin Level: Less than 0.001 ng/μg antibody, as determined by LAL assay. Aggregation: Less than 10%, as determined by HPLC. Glucocorticoid-induced tumor necrosis factor receptor family-related gene (GITR) is a member of the tumor necrosis factor receptor (TNFR) family that is expressed at low levels on unstimulated T cells, B cells, and macrophages. Upon activation, CD4+ and CD8+ T cells up-regulate GITR expression, whereas immunoregulatory T cells constitutively express high levels of GITR.