PE anti-human FLT3L Antibody, FLT3L, W19353A,BioLegend,345603

Human FLT3L was initially cloned from a T cell cDNA library using a mouse probe; the human and mouse FLT3L proteins share 72% amino acid identity. FLT3L is synthesized as a type I membrane-bound protein, which is cleaved to become a soluble growth factor. An additional soluble form of FLT3L has been reported as a result of alternative splicing. TACE (ADAM17) plays a key role in the ectodomain shedding of FLT3L. In fact, serum FLT3L levels are decreased in TACE deficient mice.FLT3L is crucial for the development of the two main subsets of dendritic cells (DCs): conventional DCs (cDCs) and plasmacytoid DCs (pDCs). Changes in the development or number of DCs can alter T cell immunity and tolerance. A feedback loop between DCs and Tregs is regulated via FLT3L, as it has been shown that the increase in Tregs induced by DC expansion delays the onset of type 1 autoimmune diabetes and IBD in mice. FLT3L also facilitates formation of Tregs and thus, reduces severity of antigen-induced arthritis in mice. FLT3L deficiency in humans has been shown to result in bone marrow hypoplasia, with low levels of hematopoietic progenitors (particularly myeloid and B cell progenitors). FLT3L is elevated in the synovial fluid of rheumatoid arthritis (RA) patients and FLT3L has been included in panels of preclinical markers for predicting the possible development of RA. The innate sensing pathway triggered by Plasmodium infection regulates DC homeostasis and adaptive immunity via FLT3L release. High levels of FLT3L and increased DCs have been detected in humans and mice during Plasmodium infection.