mProX™ Human LILRB1 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

Target Research Area

Infectious Research

Related Diseases

Human Cytomegalovirus Infection; Malaria

Gene ID

Human:10859

UniProt ID

Human:Q8NHL6

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

LILRB1, or leukocyte immunoglobulin-like receptor subfamily B member 1, has various applications in different fields. In the context of cancer immunotherapy, LILRB1 has gained attention as a potential target for immune checkpoint therapy. It is expressed by immune cells such as macrophages, cytotoxic lymphocytes, T cells, and natural killer cells, and its interaction with human leukocyte antigen (HLA) class I molecules regulates immune responses. LILRB1 acts as a phagocytosis checkpoint on macrophages by recognizing HLA class I, inhibiting the phagocytic uptake of cancer cells. Blocking the HLA class I:LILRB1 axis may enhance phagocytosis by macrophages and promote cytotoxic functions of T cells and natural killer cells. LILRB1-specific antibodies are currently being developed for pre-clinical and clinical use in cancer immunotherapy. In the context of sickle cell disease, genetic polymorphisms of HLA-F and LILRB1 have been associated with alloimmunization susceptibility in patients receiving red blood cell transfusions. These polymorphisms affect the expression levels of HLA-F and LILRB1 proteins, which are involved in immune tolerance mechanisms. Understanding these genetic factors can help optimize blood product compatibility and improve patient outcomes. Additionally, LILRB1 has been studied in the context of ulcerative colitis, a chronic inflammatory bowel disease. Gene expression analysis has identified LILRB1 as one of the key genes associated with the severity of ulcerative colitis. It is involved in inflammation, migration, and invasion of synovial tissue-derived fibroblasts through the activation of the ERK/JNK signaling pathway. Finally, LILRB1 has been investigated as a potential therapeutic target in joint inflammation of rheumatoid arthritis. Soluble LILRA3, a receptor related to LILRB1, is increased in the synovial fluid and serum of rheumatoid arthritis patients and promotes the activation, migration, and invasion of fibroblast-like synoviocytes. These findings suggest that targeting LILRB1/LILRA3 may have therapeutic implications in various diseases, including cancer, sickle cell disease, ulcerative colitis, and rheumatoid arthritis.

Protocols

Please visit our protocols page.

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FAQ

chat Skyler Garcia (Verified Customer)

How does LILRB1 interact with HLA class I molecules? Jan 21 2021

chat Patrick Liam (Creative Biolabs Scientific Support)

LILRB1 binds to HLA class I molecules, and this interaction is influenced by the structure of LILRB1's membrane-proximal Ig-like domains. Jan 21 2021

chat Casey Davis (Verified Customer)

What is the role of LILRB1 in immune responses? Nov 26 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

LILRB1 can modulate immune responses, as evidenced by its interaction with HLA-B27 homodimers and free H chains, which are stronger ligands for LILRB1 than classical HLA class I. Nov 26 2022

Published Data

Fig.1 An anticipated elevation in pSHP-1 levels and decreased phagosome acidification during ADE was observed in THP-1.2R due to the overexpression of LILRB1.

At 2 hours post-infection (hpi), pHrodo and AF488 were assessed in THP-1.2R cells following overexpression of LILRB1, with normalization to DENV infection in THP-1.2R cells transfected with an empty vector. LILRB1 or pSHP-1 levels relative to GAPDH or SHP-1 were indicated below the Western blot, and each virus particle was represented by a single dot. The data were expressed as mean ± s.d. from two independent experiments, with statistical significance indicated as ***P < 0.0001 and **P < 0.01.

Ref: Ong, Eugenia Z., et al. "Dengue virus compartmentalization during antibody-enhanced infection." Scientific Reports 7.1 (2017): 40923.

Pubmed: 28084461

DOI: 10.1038/srep40923

Research Highlights

Zeller, Tobias. et al. "Perspectives of targeting LILRB1 in innate and adaptive immune checkpoint therapy of cancer." Frontiers in immunology, 2023.
The use of immune checkpoint blockade in tumor immunotherapy has shown promising results. Blocking inhibitory pathways in T cells has been effective in treating different types of cancer and has potential to also stimulate innate immune responses. A novel emerging target for this therapy is leukocyte immunoglobulin-like receptor subfamily B member 1 (LILRB1), which exerts inhibitory functions and is expressed by immune cells such as macrophages and cytotoxic lymphocytes. By blocking the interaction between LILRB1 and human leukocyte antigen (HLA) class I molecules, the phagocytic ability of macrophages may be enhanced, as well as the cytotoxic functions of T cells and natural killer (NK) cells. Ongoing research and development of LILRB1-specific antibodies highlights its potential as a promising target for cancer immunotherapy.
Zeller, Tobias. et al. "Perspectives of targeting LILRB1 in innate and adaptive immune checkpoint therapy of cancer." Frontiers in immunology, 2023.
Pubmed: 37781391 DOI: 10.3389/fimmu.2023.1240275

Bernit, Emmanuelle. et al. "HLA-F and LILRB1 Genetic Polymorphisms Associated with Alloimmunisation in Sickle Cell Disease." International journal of molecular sciences, 2023.
The use of red blood cell (RBC) transfusion is vital for managing the acute and chronic complications of sickle cell disease (SCD). However, a major limitation of transfusion is patient alloimmunisation, which can aggravate anemia and result in delayed haemolytic transfusion reactions or transfusion deadlock. While risk factors for immunisation have been identified, accurately predicting patient alloimmunisation remains challenging. This study aimed to investigate genetic factors related to alloimmunisation in order to optimize the selection of compatible blood products and ensure adequate supplies. Previous research has shown that human leukocyte antigen Ib (HLA-Ib) molecules, such as HLA-G, -E, and -F, play a role in tolerance mechanisms. These molecules interact with specific immune effector cell receptors (LILRB1, LILRB2, and KIR3DS1) and their genetic polymorphisms have been associated with varying levels of expression and modulation of inflammatory and immune responses. The hypothesis of this study was that genetic variations in these molecules and receptors may contribute to alloimmunisation in SCD patients receiving RBC transfusions.
Bernit, Emmanuelle. et al. "HLA-F and LILRB1 Genetic Polymorphisms Associated with Alloimmunisation in Sickle Cell Disease." International journal of molecular sciences, 2023.
Pubmed: 37686397 DOI: 10.3390/ijms241713591