1. Recombinant Proteins
  2. Immune Checkpoint Proteins
  3. Stimulatory immune checkpoint molecules
  4. LIGHT & HVEM/ LT-beta-R/DcR3

LIGHT & HVEM/ LT-beta-R/DcR3

LIGHT (TNFSF14/CD258), a type II transmembrane glycoprotein, is a homologous to lymphotoxins, with inducible nature and the ability to compete with herpes simplex virus glycoprotein D for herpes virus entry mediator (HVEM). LIGHT is a tumor necrosis factor (TNF) superfamily ligand which regulates T cell immune responses by signaling through two primary functional receptors, the HVEM and the lymphotoxin beta receptor (LT-beta-R). LIGHT is expressed on activated T cells, NK cells, monocytes, granulocytes, and immature dendritic cells (DCs); HVEM is expressed on resting T cells, NK cells, monocytes, immature DCs, and endothelial cells; LT-beta-R is expressed on DCs, endothelial cells, and stromal cells but is not expressed on lymphocytes. LIGHT is also trapped by non-functional soluble decoy receptor 3 (DcR3), which is highly expressed in various human tumors, such as multiple myeloma and diffuse large B-cell lymphoma. As a co-stimulator of T cells, on engagement with LT-beta-R, LIGHT induces cytotoxicity against some human cancer cells, and promotes cytokine production and the release of the naive T cell-attracting chemokines in stromal cells, thus leading to the increased presence of lymphocytes in tissues. In addition, triggering of HVEM signals on T cells by LIGHT co-stimulates T cell proliferation and interferon IFN-gamma secretion in response to T cell receptor engagement, leading to enhanced T cell immunity. LIGHT has been in pre-clinical development for over a decade and shows promise as a modality of enhancing treatment approaches in the field of cancer immunotherapy.

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