GITRL Extracellular Domain (human, recombinant)

AITRL|Glucocorticoid-induced TNF-Related Ligand|TNFSF18|Tumor Necrosis Factor Ligand Superfamily Member 18

Glucocorticoid-induced TNF-related ligand (GITRL), also known as TNF superfamily member 18 (TNFSF18), is a type II transmembrane glycoprotein and member of the TNF superfamily with roles in adaptive immunity.{56065} It is composed of an N-terminal cytoplasmic domain, a transmembrane domain, and a C-terminal extracellular domain that binds to its receptor GITR (Item No. 32017) on T cells to regulate their activity. GITRL is expressed on professional and non-professional antigen-presenting cells, including B cells, monocytes, unstimulated myeloid dendritic cells, and plasmacytoid dendritic cell precursors, as well as microvascular-derived endothelial cells. GITRL co-stimulation increases activation and proliferation of T cell receptor-triggered effector T cells. It also enhances the activity of effector T cells by binding to regulatory T cells and inhibiting their activity. Upregulation of dendritic cell Gitrl levels suppresses regulatory T cell function, enhances effector T cell function, and delays tumor progression in a murine Lewis lung carcinoma model.{53754} Serum and synovial fluid levels of GITRL are increased and positively correlated with autoantibody production in patients with rheumatoid arthritis.{53755} Serum levels of GITRL are positively correlated with disease progression in patients with Sjögren syndrome.{53756} Cayman’s GITRL Extracellular Domain (human, recombinant) protein is a disulfide-linked homodimer. The reduced monomer, comprised of the GITRL extracellular domain (amino acids 72-199) fused to mouse IgG2a Fc at its C-terminus, consists of 361 amino acids and has a calculated molecular weight of 40.9 kDa. As a result of glycosylation, the monomer migrates at approximately 45 kDa by SDS-PAGE under reducing conditions.

-80

-80

Lyophilized from sterile PBS, pH 7.4

365

≥90% estimated by SDS-PAGE