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Validated All-in-One™ qPCR Primer for LILRB1(NM_006669.7) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
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. 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. [provided by RefSeq].
Gene References into function
- effect on cytokine production by antigen-stimulated T cells
- Engagement of ILT2/CD85j found in Sezary syndrome cells inhibits their CD3/TCR signaling.
- Increased binding to influenza virus-infected cells is observed in leukocyte Ig-like receptor-1 (LIR1) that is functional and possibly results from the generation of complexes of class I MHC proteins after influenza virus infection.
- inhibitory receptors Ig-like transcript 2 (ILT2) and ILT4 compete with CD8 for MHC class I binding and bind preferentially to HLA-G
- Invariant receptor CD85j expressed on CD8+ T cells mediates the specific recognition of an infectious antigen component and provides a novel example that extends the characteristics of innate immunity to cells mainly involved in adaptive immunity.
- C-terminal Src kinase is regulated by the leukocyte inhibitory receptor CD85j
- Cell surface expression of immunoglobulin-like inhibitory MHC class I receptor CD85j is associated with T cell engagement into various stages of the cytolytic differentiation pathway.
- report that ILT2 receptor, ILT3 receptor, ILT4 receptor, and KIR2DL4 receptor expression is up-regulated by HLA-G histocompatibility antigen in antigen-presenting cells, natural killer cells, and T cells
- CD85j prevents the rescue from apoptosis and the cooperation between dendritic cells and antigen-specific T cells that is mediated by human osteoclast-associated receptor (hOSCAR).
- Polymorphism in LILRB1 is associated with susceptibility to rheumatoid arthritis with HLA-DRB1 shared epitope negative subjects
- Coexpression of ILT2 with killer cell immunoglobulin-like receptor (KIR) in human natural killer (NK) cells may compensate for weak interactions between particular KIR and major histocompatibility complex-I (MHC-I).
- Kinetic studies demonstrated that LILRB1 binds to MHCIs with fast association and dissociation rates, typical of cell-cell recognition receptors.
- Blocking HLA-G receptors ILT2 and ILT4 prevents HLA-G inhibitory effects, leading to the conclusion that that HLA-G acts mainly through these receptors.
- results show that the peripheral blood mononuclear cells from some patients with systemic lupus erythematosus show a defective expression of ILT2, and that most of them exhibit a poor function of this inhibitory receptor
- Progenitor mast cells expressed cell surface inhibitory LILRB1. Mature cord-blood-derived mast cells had detectable mRNA encoding multiple LILRs, none were expressed on the cell surface.
- ligation of LILRB1 on dendritic cells by self-HLA molecules may play a key role in controlling the balance between the induction and suppression of adaptive immune responses
- CD85j(+) NK cell inhibition of HIV-1 replication in MDDC is mainly mediated by CD85j interaction with an unknown ligand
- The presence of LILRB1 in placental stromal cells and LILRB2 in vascular smooth muscle strongly suggest that HLA-G has novel functions in regulation of placental immunity, development and function of the extraembryonic vasculature.
- The 2.2-A structure of a LIR-1/UL18/peptide complex reveals increased contacts and optimal surface complementarity in the LIR-1/UL18 interface compared with LIR/MHCI interfaces, resulting in a >1,000-fold higher affinity.
- Natural killer (NK) cells are targets which express relatively high amounts of inhibitory ILT2/CD85j receptors on the cell surface, capable of shaping interferon-gamma release in response to viral products and during NK and dendritic cell cross-talk.
- Expressed on cultured osteoclast precursor cells derived from peripheral blood monocytes; LILRB1 could be inhibitory for osteoclast development in presence of receptor activator of NF-kappaB ligand (RANKL) and macrophage colony stimulating factor (M-CSF)
- CD85j(leukocyte Ig-like receptor 1) is expressed in Polymyositis and sporadic Inclusion body myositis at the sites of partial invasion and in Dermatomyositis in perivascular inflammation
- Human inhibitory receptor immunoglobulin-like transcript 2 amplifies CD11b+Gr1+ myeloid-derived suppressor cells that promote long-term survival of allografts.
- soluble HLA-G dimer up-regulates inhibitory receptor ILT2 on alloreactive CD8+ T cells