Preferred Label : CXCR3/IL-12/TGFb1 Inhibitor Engineered Oncolytic Vaccinia Virus VET3-TGI;
NCIt synonyms : CXCR3/IL-12/TGFb1 Inhibitor Engineered Oncolytic VV VET3-TGI; CXCR3/IL-12/TGF-beta Inhibitor Engineered Oncolytic Vaccinia Virus VET3-TGI;
NCIt definition : An oncolytic vaccinia virus (VV) genetically engineered to express C-X-C chemokine
receptor type 3 (CXCR3), the human pro-inflammatory cytokine interleukin-12 (IL-12),
and an inhibitor of transforming growth factor (TGF)-beta 1 (TGFb1; TGF-b1), with
potential immunomodulating and antineoplastic activities. Upon administration of CXCR3/IL-12/TGFb1
inhibitor engineered oncolytic VV VET3-TGI, the virus preferentially targets, infects
and replicates in tumor cells, particularly tumor cells expressing CXCR3 ligands,
causing oncolysis. In turn, the lysed tumor cells release various tumor-associated
antigens (TAAs), which induce an immune response against the tumor cells. In addition,
CXCR3/IL-12/TGFb1 inhibitor engineered oncolytic VV VET3-TGI promotes the secretion
of IL-12 and the TGFb1 inhibitor in the tumor microenvironment (TME). IL-12 activates
natural killer cells (NKs), induces the secretion of interferon-gamma (IFNg) and promotes
CD8 cytotoxic T-lymphocyte (CTL) responses against tumor cells, which may result in
immune-mediated tumor cell death and inhibition of tumor cell proliferation. The inhibition
of TGFb1 prevents TGFb1-mediated signaling. This abrogates TGFb1-mediated immunosuppression,
enhances anti-tumor immunity in the TME and further promotes CTL-mediated immune response
against tumor cells. The TGF-beta signaling pathway is often deregulated in tumors
and plays a key role in immunosuppression in the TME. TGFb1 is the predominant isoform
in many tumors.;
Molecule name : VET3-TGI; VET3 TGI;
Origin ID : C211499;
concept_is_in_subset
