CD137/TNFRSF9/4-1BB
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Introduction To CD137/TNFRSF9/4-1BB
Drug targets a biomolecule that can directly bind to drugs and then react. Generally, the target refers to a protein, which is related to the cause of disease. The focus of the target began with focusing on tumors, and then began to spread to various fields .CD137/TNFRSF9/4-1BB protein is a common target in medicine.
CD137, also known as 4-1BB, is a receptor for T cell stimulation of expression and is a member of the TNFRSF giant family. There are various types of activated CD cells, natural killer cells T cells, and other immune-related cells.CD137 can be expressed only on already activated T cells and does not occur on T cells that are not activated. Expression also occurs on the surface of other immune cells.
Function of Target CD137/TNFRSF9/4-1BB
CD137 on the surface of T cells would react with CD137L on APCs and then destimulate the two cells already producing the response. CD137 induced differentiation and growth of T cells and APCS with increased secretion of cytokines. CD137 preempts CD8 + T cells, preventing CD8 + T cell-induced AICD. The expression level of CD137 in cells is also affected by different TCR affinities, and the different intensity and type of stimulation can also alter CD137L expression. Signaling between the appearance of CD137 / CD137L may also mitigate the effects of T cells in producing an immune response, prevent T cell activation and proliferation, and reduce cytokine production. When CD137 is not expressed on the surface of T cells, T cells and myeloid cells will overproliferate. This may be because the signal transmitted by CD137 itself causes some kind of regulatory molecule by DCs, or possibly due to the inhibitory signal from CD137L to T cells.
Soluble CD137 (sCD137) is a soluble form of CD137 without synergistic stimulatory activity. Human sCD137, generated by differential splicing, simultaneously acts as a negative regulator-dependent CD137L to antagonize the batch-stimulating activity of CD137 to inhibit effector T-cell proliferation. In hypoxia and autoimmune diseases, serum sCD137 levels are increased in patients such as malignancy, rheumatoid arthritis, and mandatory spondylitis.
In CD137, under the influence of some unknown factors, it will produce some abnormal immune responses, which will cause the body's immune system to lose control and produce an immune response to its substances and cause harm to the body. If no stimulatory signal is generated, T cells that have already reacted to the antigen will not be activated, causing themselves to develop immune tolerance, severely leading to apoptosis. If the stimulation produced exceeds a certain limit, the autoreactive cell activity will be enhanced.CD137 / CD137L co-stimulatory signaling is one of the main drivers of type 1 cell-mediated immune responses, involving a variety of autoimmune diseases, including systemic lupus erythematosus (SLE) rheumatoid arthritis (RA) type 1 diabetes mellitus (TID) ankylosing spondylitis.
Gene Pathway of Target CD137/TNFRSF9/4-1BB
The binding of CD137 and its ligands clusters TRAF 1 and TRAF 2 activates NF- ᴋB and MAP kinase signaling pathways, ultimately leading to IL-2 and IFN- γ secretion and upregulation of the antiapoptotic molecules Bcl-xL and Bfl-1.
Fig 1: CD137 Gene Pathway. (Reference documentation: Xu MM, Ménoret A, Nicholas SE, Günther S, Sundberg EJ, Zhou B, Rodriguez A, Murphy PA, Vella AT. Direct CD137 costimulation of CD8 T cells promotes retention and innate-like function within nascent atherogenic foci. Am J Physiol Heart Circ Physiol. 2019 Jun 1;316(6):H1480-H1494. )
Alpha Lifetech Can Provide
| Catalog Number | Product Name | Product Sizes |
|---|---|---|
| ALP64693 | 50ug,100ug,500ug | |
| ALP64643 | 50ug,100ug,500ug | |
| ALP64642 | 50ug,100ug,500ug | |
| ALP64615 | 50ug,100ug,500ug | |
| ALP64570 | 50ug,100ug,500ug | |
| ADT1682 | ADT1682-Urelumab Biosimilar– Anti-TNFRSF9, CD137 mAb – Research Grade |
1mg,5mg |
| ADT1685 | ADT1685-Utomilumab Biosimilar– Anti-Human TNFRSF9 mAb – Research Grade |
1mg,5mg |
Reference
[1] Pichler AC, Carrié N, Cuisinier M, Ghazali S, Voisin A, Axisa PP, Tosolini M, Mazzotti C, Golec DP, Maheo S, do Souto L, Ekren R, Blanquart E, Lemaitre L, Feliu V, Joubert MV, Cannons JL, Guillerey C, Avet-Loiseau H, Watts TH, Salomon BL, Joffre O, Grinberg-Bleyer Y, Schwartzberg PL, Lucca LE, Martinet L. TCR-independent CD137 (4-1BB) signaling promotes CD8+-exhausted T cell proliferation and terminal differentiation. Immunity. 2023 Jul 11;56(7):1631-1648.e10.
[2] Otano I, Azpilikueta A, Glez-Vaz J, Alvarez M, Medina-Echeverz J, Cortés-Domínguez I, Ortiz-de-Solorzano C, Ellmark P, Fritzell S, Hernandez-Hoyos G, Nelson MH, Ochoa MC, Bolaños E, Cuculescu D, Jaúregui P, Sanchez-Gregorio S, Etxeberria I, Rodriguez-Ruiz ME, Sanmamed MF, Teijeira Á, Berraondo P, Melero I. CD137 (4-1BB) costimulation of CD8+ T cells is more potent when provided in cis than in trans with respect to CD3-TCR stimulation. Nat Commun. 2021 Dec 15;12(1):7296.
[3] Xu MM, Ménoret A, Nicholas SE, Günther S, Sundberg EJ, Zhou B, Rodriguez A, Murphy PA, Vella AT. Direct CD137 costimulation of CD8 T cells promotes retention and innate-like function within nascent atherogenic foci. Am J Physiol Heart Circ Physiol. 2019 Jun 1;316(6):H1480-H1494.
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2018-07-16
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