Recombinant Human sTNF-RII (TNFRSF1B) (carrier-free)
Description
The biological effects of TNF are mediated by two cell surface TNF receptors, TNF-RI and TNF-RII. TNF-RI and TNF-RII are structurally related but functionally distinct. Also, TNF-RI is widely expressed on most cells, whereas TNF-RII is more restricted and is primarily expressed in hematopoietic cells and cells of the immune system. The function of TNF-RII is less understood and has fewer biological effects than TNF-RI. Unlike TNF-RI, TNF-RII does not have death domain and will induce NF-κB activation through a different pathway. It is generally accepted that TNF-RI induces both apoptosis and survival pathways and TNF-RII induces only survival pathway. Only membrane-bound TNF can active TNF-RII effectively. Soluble TNF can bind TNF-RII but can not induce TNF-RII signaling. Upon binding of TNF, TNF-RII will form a trimer and recruit TRAF2, therefore leading to activation of NF-κB. In T cells, TNF-RII costimulation provides survival signals during the differentiation program trigger by TCR-mediated stimulation and also during clonal expansion in response to intracellular bacterial pathogens. Both TNF-RI and TNF-RII can be released from cell surface by ectodomain shedding. The resulting soluble TNF-RI and TNF-RII can bind TNF with high affinity and modulate TNF effects. An in vitro study showed that both TNF-RI and TNF-RII are constitutively released from monocytes. LPS stimulation can further increase soluble TNF-RII release. It has been reported that association of TNF-RII polymorphism with some lymphomas, solid tumors, and autoimmune diseases. The plasma level of soluble TNF-RII is increased in obese people and is related to insulin resistance. In addition, recombinant Fc-tagged soluble TNF-RII has been used to treat rheumatoid arthritis.