mProX™ Human LILRB4 Stable Cell Line

Product Information

Target Family

Oncology

Target Protein Species

Human

Host Cell Type

HEK293;CHO-K1;THP-1

Target Classification

Oncology Cell Lines

Gene ID

Human:11006

UniProt ID

Human:Q8NHJ6

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

LILRB4, also known as ILT3 or gp49B, has various applications in different fields. In the context of acute lymphoblastic leukemia (ALL), LILRB4 is implicated in acquired resistance to DOT1L inhibition, a potential therapeutic target for KMT2A-rearranged ALL. The loss of dependency on DOT1L-mediated H3K79 methylation in resistant cells is accompanied by the upregulation of LILRB4 and other myeloid-associated genes. In the field of infectious diseases, LILRB4 is involved in regulating the function of decidual myeloid-derived suppressor cells (dMDSCs) during Toxoplasma gondii infection. The downregulation of LILRB4 expression on dMDSCs leads to the dysfunction of these cells, potentially contributing to adverse pregnancy outcomes. In non-small cell lung cancer (NSCLC), high expression of LILRB4 on tumor-infiltrating cells, including myeloid-derived suppressor cells (MDSCs), is associated with poor prognosis and shorter overall survival and relapse-free survival. LILRB4 promotes tumor evasion and cancer progression in NSCLC. Additionally, LILRB4 is implicated in the development of myelomatous effusion (ME), a rare manifestation of extramedullary multiple myeloma (MM). Single-cell RNA sequencing analysis reveals the expression of LILRB4 in extramedullary-initiating cells (EMICs) associated with increased cellular proliferation and poor prognosis in MM. Furthermore, LILRB4 on NK cells interacts with fibronectin on target cells to attenuate natural cytotoxicity, suggesting a potential role in regulating NK cell activity in the tumor microenvironment.

Protocols

Please visit our protocols page.

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FAQ

chat Alex Davis (Verified Customer)

How does LILRB4 influence tumor metastasis? Dec 23 2020

chat Patrick Liam (Creative Biolabs Scientific Support)

LILRB4 orchestrates the polarization of myeloid-derived suppressor cells (MDSCs) to exhibit pro-tumor phenotypes and promotes MDSC-mediated tumor metastasis. Dec 23 2020

chat Cameron Miller (Verified Customer)

What is the impact of LILRB4 on immune responses in solid tumors? May 10 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

LILRB4 suppresses antitumor immunity in solid tumors, and its genetic deletion or antibody treatment modulates immune cells to enhance survival against tumor challenge. May 10 2022

Published Data

Fig.1 The activation of STAT3 and the inhibition of NF-κB through SHP-1 are initiated by the interaction between Gal-8 and LILRB4.

To demonstrate the function of Gal-8/LILRB4 more effectively, a LILRB4-knockdown (KD) THP-1 cell line was created through the utilization of shRNA lentivirus (designated as THP-1 shLILRB4), while a control cell line (THP-1 NC) was established using cargo lentivirus. Various concentrations of Gal-8 were introduced to THP-1 cells (whether they were control or LILRB4-KD), and subsequent Western Blot detection revealed the significant phosphorylation of downstream phosphatases. Remarkably, in control THP-1 cells treated with Gal-8, SHP-1 (although not SHP-2 or SHIP-1) exhibited substantial phosphorylation. However, in LILRB4-KD THP-1 cells, the phosphorylation of SHP-1 was considerably diminished.

Ref: Wang, Yiting, et al. "Galectin-8 is a major ligand of LILRB4 prompting MDSC functions in the tumor microenvironment." Biorxiv (2022): 2022-07.

Pubmed: NA

DOI: 10.1101/2022.07.27.501694

Research Highlights

Schneider, Pauline. et al. "Modelling acquired resistance to DOT1L inhibition exhibits the adaptive potential of KMT2A-rearranged acute lymphoblastic leukemia." Experimental hematology & oncology, 2023.
In cases of KMT2A-rearranged acute lymphoblastic leukemia (ALL), a highly aggressive form of cancer, the oncogenic KMT2A-fusion proteins are responsible for recruiting DOT1L, leading to the development of the disease. This highlights the potential of targeting DOT1L as a therapeutic approach. However, the first-in-class DOT1L inhibitor pinometostat used for treatment often results in non-responsiveness. To gain insight into this issue, a study was conducted in which acquired pinometostat resistance was observed in pediatric KMT2A::AFF1-rearranged ALL cells. Further analysis revealed that resistance was likely mediated by dysregulation of Wnt/beta-catenin signaling, caused by a loss of DOT1L-dependent H3K79 methylation.
Schneider, Pauline. et al. "Modelling acquired resistance to DOT1L inhibition exhibits the adaptive potential of KMT2A-rearranged acute lymphoblastic leukemia." Experimental hematology & oncology, 2023.
Pubmed: 37740239 DOI: 10.1186/s40164-023-00445-8

Li, Yuantao. et al. "LILRB4 regulates the function of decidual MDSCs via the SHP-2/STAT6 pathway during Toxoplasma gondii infection." Parasites & vectors, 2023.
The infection caused by Toxoplasma gondii is known to have adverse effects on pregnancy, such as recurrent abortion, fetal growth restriction and malformations in infants. At the fetal-maternal interface, a type of immunosuppressive cell called decidual myeloid-derived suppressor cells (dMDSCs) are responsible for maintaining a healthy pregnancy. These dMDSCs express the inhibitory molecule leukocyte immunoglobulin-like receptor B4 (LILRB4), which is crucial for their role in pregnancy. Recent studies have shown that T. gondii infection can result in a downregulation of LILRB4 on decidual macrophages, raising questions about the potential dysfunction of dMDSCs due to altered LILRB4 expression.
Li, Yuantao. et al. "LILRB4 regulates the function of decidual MDSCs via the SHP-2/STAT6 pathway during Toxoplasma gondii infection." Parasites & vectors, 2023.
Pubmed: 37461040 DOI: 10.1186/s13071-023-05856-4