Rabbit Anti-Human LILRB4 (internal) Polyclonal antibody

Name: Rabbit Anti-Human LILRB4 (internal) Polyclonal antibody
SKU: DPABH-08862
Rating: 5 (1 reviews)

Rabbit Anti-Human LILRB4 (internal) Polyclonal antibody for IF

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COA

SDS

Datasheet

Key features and details

Target: LILRB4
Host: Rabbit
Application: IF
Species Reactivity: Human

Summary

Specifications

Antibody Isotype

IgG

Species Reactivity

Human

Immunogen

Synthesized peptide derived from internal of human LILRB4.

Conjugate

Unconjugated

Applications

Application Notes

IF: 1:100-1:500

General Notes

This product (Catalog No. DPABH-08862) is a rabbit-derived IgG polyclonal antibody raised against human LILRB4. It has been affinity purified by protein A. This gene is a member of the leukocyte immunoglobulin-like receptor (LIR) family, which is found in a gene cluster at chromosomal region 19q13.4. The encoded protein belongs to the subfamily B class of LIR receptors which contain two or four extracellular immunoglobulin domains, a transmembrane domain, and two to four cytoplasmic immunoreceptor tyrosine-based inhibitory motifs (ITIMs). The receptor is expressed on immune cells where it binds to MHC class I molecules on antigen-presenting cells and transduces a negative signal that inhibits stimulation of an immune response. The receptor can also function in antigen capture and presentation. It is thought to control inflammatory responses and cytotoxicity to help focus the immune response and limit autoreactivity. Multiple transcript variants encoding different isoforms have been found for this gene.
DPABH-08862 is suitable for use in IF (immunofluorescence) (1:100–1:500) application.
DPABH-08862 is supplied as a liquid formulation in PBS (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. For long-term storage, keep at −20 °C. For short-term use, store at 2–8 °C. Avoid repeated freeze–thaw cycles to maintain antibody integrity and performance.

Target

Alternative Names

Leukocyte immunoglobulin-like receptor subfamily B member 4; Leukocyte immunoglobulin-like receptor 5; LIR-5; Immunoglobulin-like transcript 3; ILT-3

Entrez Gene ID

11006

UniProt ID

Q8NHJ6

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Immune Checkpoint Inhibitors in Acute Myeloid Leukemia: Novel Combinations and Therapeutic Targets

CURRENT ONCOLOGY REPORTS

Authors: Stahl, Maximilian; Goldberg, Aaron D.

Abstract

Purpose of ReviewImmune checkpoint therapy has dramatically changed the therapeutic landscape of solid malignancies. Here, we review the scientific rationale and current data evaluating immune checkpoint inhibitors in acute myeloid leukemia (AML).Recent FindingsImmune checkpoint inhibitor monotherapy has shown limited clinical activity in AML. Initial results from early-phase clinical trials suggest that rational combinations of immune checkpoint inhibition with hypomethylating agents (HMAs) are safe and potentially more promising. There are currently no data directly comparing immune checkpoint inhibition to standard therapies. Emerging immune targets more specific for leukemia cells including LILRB4 may improve future therapeutic efficacy.SummaryThe success of immune checkpoint inhibition in AML has been modest to date. However, an improved understanding of the biology and the use of rational combinations has potential to improve rates of durable responses. Multiple clinical trials in AML are currently evaluating the use of immune checkpoints alone and in combination.

Numerical and functional defects in CD8(+)CD28(-) T-suppressor lymphocytes from patients with primary immune thrombocytopenia

BRITISH JOURNAL OF HAEMATOLOGY

Authors: Li, Huiyuan; Hao, Yating; Zhang, Donglei; Liu, Wenjie; Li, Yang; Lyu, Mingen; Fu, Rongfeng; Xue, Feng; Liu, Xiaofan; Yang, Renchi

Abstract

Primary immune thrombocytopenia (ITP) is an acquired autoimmune disorder, and loss of immune tolerance has been implicated in ITP pathogenesis. CD8(+)CD28(-) suppressor (Ts) cells have an immunosuppression function and are involved in several autoimmune disorders. However, the role of Ts cells in ITP is currently not clear. Here, flow cytometry was used to detect the CD8(+)CD28(-)CD127(-) proportion, which was decreased in active ITP patients compared with that of controls. Function analysis showed that immunosuppression of CD8(+)CD28(-) Ts cells in ITP patients was impaired. Mechanistic studies have shown that CD8(+)CD28(-) Ts cells from controls can downregulate CD80 and upregulate LILRB4 (ITL3) and LILRB2 (ILT4) expression on CD14(+) monocytes, whereas these abilities were not found in Ts cells from ITP patients. Furthermore, Inducible T-cell costimulatory (ICOS) expression on the Ts cell surface after activation was decreased whereas programmed death 1 and interleukin 10 expression was not changed in ITP patients compared with those of controls. In summary, the down-regulated quantity and function of Ts cells in active patients indicated that a Ts defect was involved in ITP. Moreover, decreased ICOS expression and the loss of the ability to regulate co-stimulator expression on antigen-presenting cells partly explained the defective Ts-mediated suppression.