Psychiatry related information on LILRA2

• In functional studies, LIR-7 suppressed innate host defense mechanisms by shifting monocyte production from interleukin-12 toward interleukin-10 and by blocking antimicrobial activity triggered by Toll-like receptors [1].

High impact information on LILRA2

• We have identified two cell subsets in human blood based on the lack of lineage markers (lin-) and the differential expression of immunoglobulin-like transcript receptor 1 (ILT1) and ILT3 [2].
• However, staining in the presence of antibodies reactive with ILT receptors revealed that the interaction of HLA-G tetramers with blood monocytes was largely due to binding to ILT4 [3].
• Immunoglobulin-like transcript (ILT) 3 is a novel cell surface molecule of the immunoglobulin superfamily, which is selectively expressed by myeloid antigen presenting cells (APCs) such as monocytes, macrophages, and dendritic cells [4].
• Thus, LIR7 is an activating receptor for eosinophils that elicited the release of cytotoxic granule proteins, de novo lipid mediator generation, and cytokine release through vesicular transport [5].
• Cross-linking of LIR7 with plate-bound antibody elicited the dose- and time-dependent release of eosinophil-derived neurotoxin and leukotriene C(4) [5].

Biological context of LILRA2

• Furthermore, ILT1 and ILT2 are encoded on chromosome 19, as are Fc alphaR and KIR [6].
• One ILT, designated ILT1, contains a short cytoplasmic domain that lacks sequence motifs implicated in signal transduction [7].
• Using the sequence data produced by the human genome project, we have developed a hypothesis that reconstructs the genesis of the two human ILT clusters in detail which will help to understand the function of the LRC [8].
• A human cDNA clone cross-hybridizing to a murine p91 probe was isolated from a human spleen cDNA library, and was found to code for a molecule quite similar to members of the immunoglobulin-like transcript (or ILT) family [9].

Anatomical context of LILRA2

• Eosinophils activated with antibodies to LIR7 embedded in gel-phase EliCell preparations showed leukotriene C(4) generation at the nuclear envelope and the release of IL-12 but not IL-4 by vesicular transport [5].
• Several members of the immunoglobulin-like transcript (ILT), also called leukocyte immunoglobulin-like receptor (LIR), family of transmembrane proteins have been identified as receptors for class I HLA molecules and transduce inhibitory signals to leukocytes upon binding of these ligands [10].
• Expression levels of certain ILT molecules allow definition of blood monocyte and dendritic cell (DC) subsets [11].
• Some mast cells and endothelial cells expressed LIR-7 [12].
• The HLA-G-ILT (immunoglobulin-like transcript) interaction leads to development of tolerogenic DC with the induction of anergic and immunosuppressive T cells [13].

Associations of LILRA2 with chemical compounds

• We identified LIR7, an activating member coupled to the common Fc receptor gamma chain, and LIR3, an inhibitory member containing cytoplasmic immunoreceptor tyrosine-based inhibitory motifs, on these cells from human peripheral blood [14].
• ILT1 has an arginine within the transmembrane region, followed by a short cytoplasmic tail, similar to human Fc alphaRI and bovine Fc gamma2R [6].

Physical interactions of LILRA2

• Isotypic variation of novel immunoglobulin-like transcript/killer cell inhibitory receptor loci in the leukocyte receptor complex [15].

Other interactions of LILRA2

• We investigated the transcriptional regulation of ILT1, ILT2, and ILT4 genes to elucidate control mechanisms operating on the specific expression of ILT receptors [16].

References