BAFF-R (human):Fc (human, rec.)

(3 x 50µg). The extracellular domain of human BAFF-R (amino acids 2-71) is fused at the C-terminus to the Fc portion of human IgG1. Inhibits BAFF activity. Detection of membrane-bound human and mouse BAFF in combination with PAb to human IgG1. Lyophilized. Contains PBS. BAFF is mainly produced by innate immune cells such as neutrophils, monocytes, macrophages, dendritic cells, follicular dendritic cells. T cells, activated B cells, some malignant B cells and also non-lymphoid cells like astrocytes, synoviocytes and epithelial cells can also produce BAFF. BAFF binds three distinct receptors (BAFF-R, TACI and BCMA) expressed predominantly on B cells, although activated T cells also express BAFF-R. BAFF is a master regulator of peripheral B cell survival, and together with IL-6, promotes Ig class-switching and plasma cell differentiation. Besides its major role in B cell biology, BAFF co-stimulates activated T cells. Deregulated expression of BAFF leads to autoimmune disorders in mice. In humans, elevated levels of soluble BAFF have been detected in the serum of patients with various autoimmune diseases, such as Sjögren's syndrome, Rheumatoid Arthritis (RA), Multiple sclerosis (MS) and Systemic Lupus Erythematosus (SLE). BAFF is also increased levels in some lymphoid cancers.