Introduction To ILT3/CD85k/LILRB4
Drug targets a biomolecule that can directly bind to drugs and then react. Generally, the target refers to a protein related to the cause of disease. The focus of the target began with focusing on tumors and then began to spread to various fields. Introduction to ILT3/cd85k/LILRB4 protein is a common target in medicine.
LIT 3 is a fibronectin-binding inhibitory immune receptor, also known as LILRB4, LIR-5, CD85k, and is a member of leukocyte immunoglobulin-like receptors (LILRs / LIRs), an important mediator of immune tolerance, and an inhibitory receptor expressed on activated NK cells and myeloid cells. LIT 3 contains only two extracellular immunoglobulin domains, a transmembrane domain, and three ITIMs (the immunoreceptor amino acid suppression motif). Interestingly, the gene encoding LILRB4 is in turn one of the most polymorphic of all receptor-coding genes, with at least 15 known single nucleotide polymorphisms.
Function of Target ILT3/CD85k/LILRB4
Immunoglobulin-like transcript (ILT) 3 is an immunosuppressive molecule that negatively regulates myeloid cell activation. Overexpression of ILT 3 in tumor cells induces immune escape in solid tumors and promotes the invasive immunoglobulin-like transcript of monocytic acute myeloid leukemia cells ILT 3 to be highly expressed on tumor-associated myeloid cells and promotes their suppressive phenotype. ILT 3 signals inside cells to inhibit transcription of NF-kappaB activation and costimulatory molecules and induces nonpotent and regulatory functions in T cells with cognate specificity. Both membrane and soluble ILT 3 are proteins with potent immunosuppressive activity that are important for therapeutic rejection, autoimmunity, and cancer. Ectopic expression of ILT 3 in CLL is a prominent feature of neoplastic B cells and hematopoietic stem cells, thus identifying IL ILT 3 as a selective marker for CLL malignancy.
Gene Pathway of Target ILT3/CD85k/LILRB4
ILT 3 recruits SHP 2 and SHIP 1, subsequently activates ERK 1 / 2, and signaling mediated epithelial-mesenchymal transition (EMT) and increased vascular endothelial growth factor (VE GF) -A expression in NSCLC cells, which are responsible for tumor cell motility and angiogenesis, respectively. ILT 3 signals inside the cells to inhibit tyrosine phosphorylation, NF-kappaB and MAPK p38 activity, transcription of certain co-stimulatory molecules, secretion of cytokines and chemokines, and extracellular entry into dendritic cell-interacting T cells. ILT 3 expression in CLL is driven by Deltex1, a suppressor of antigen receptor signaling in lymphocytes. The triggering of ILT 3 inhibits Akt kinase activation upon B cell receptor (BCR) stimulation, and ILT 3 may functionally contribute to the regulatory network controlling tumor progression by inhibiting the Akt pathway.

Fig 1: LILRB4 Gene Pathway. (Reference source: Itagaki F, Nakatsuka K, Sakai H, Endo S, Su MT, Takai T. Fibronectin on target cells attenuates natural cytotoxicity of NK cells via myeloid immune checkpoint ILT3/LILRB4/gp49B. Int Immunol. 2023 Jul 7;35(7):339-348.)
Alpha Lifetech Can Provide
Currently, various immune drugs targeting ILT3/CD85k/LILRB4 targets are in the updating iteration, and taking the disease alone or in combination with other products has become a new approach with remarkable achievements. The ILT3/CD85k/LILRB4 targets have shown important research value and application prospects in both biology and drug research and development. With further research and detection technology advances, ILT3/cd85k/LILRB4 target products are also essential in medical research. Alpha Lifetech can provide ILT3/CD85k/LILRB4 corresponding products and help each customer's research and development. Alpha Lifetech provides end-to-end biotechnology development solutions, from upstream cell culture optimization to downstream purification scale. Our process is validated through analytical techniques such as HPLC, SDS-PAGE, and mass spectrometry to ensure product consistency and regulatory compliance. By combining cutting-edge biotechnology expertise with flexible service models, we help clients accelerate project research progress and ensure smooth experimentation.
| Catalog Number | Product Name | Product Sizes |
|---|---|---|
| ALP64550 | 50ug,100ug,500ug | |
| ALP64548 | ALP64548-Recombinant Human ILT3/CD85k/LILRB4 Protein, Fc Tag | 50ug,100ug,500ug |
| ALP64539 | ALP64539-Recombinant Mouse ILT3/CD85k/LILRB4 Protein, Fc Tag | 50ug,100ug,500ug |
Reference
[1] Li J, Gao A, Zhang F, Wang S, Wang J, Wang J, Han S, Yang Z, Chen X, Fang Y, Jiang G, Sun Y. ILT3 promotes tumor cell motility and angiogenesis in non-small cell lung cancer. Cancer Lett. 2021 Mar 31;501:263-276.
[2] Singh L, Muise ES, Bhattacharya A, Grein J, Javaid S, Stivers P, Zhang J, Qu Y, Joyce-Shaikh B, Loboda A, Zhang C, Meehl M, Chiang DY, Ranganath SH, Rosenzweig M, Brandish PE. ILT3 (LILRB4) Promotes the Immunosuppressive Function of Tumor-Educated Human Monocytic Myeloid-Derived Suppressor Cells. Mol Cancer Res. 2021 Apr;19(4):702-716.
[3] Xu Z, Chang CC, Li M, Zhang QY, Vasilescu EM, D'Agati V, Floratos A, Vlad G, Suciu-Foca N. ILT3.Fc-CD166 Interaction Induces Inactivation of p70 S6 Kinase and Inhibits Tumor Cell Growth. J Immunol. 2018 Feb 1;200(3):1207-1219.
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2018-07-16


