LILRB4

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LILRB4
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesLILRB4, CD85K, ILT-3, ILT3, LIR-5, LIR5, leukocyte immunoglobulin like receptor B4, B4
External IDsOMIM: 604821 MGI: 102702 HomoloGene: 86756 GeneCards: LILRB4
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001291892
NM_001291893
NM_008147

RefSeq (protein)

NP_001265355
NP_001265356
NP_001265357
NP_001265358
NP_001265359

NP_001278821
NP_001278822
NP_032173

Location (UCSC)Chr 19: 54.64 – 54.67 MbChr 10: 51.36 – 51.36 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Leukocyte immunoglobulin-like receptor subfamily B member 4 is a protein that in humans is encoded by the LILRB4 gene.[5][6][7]

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 monocytic 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. LILRB4 has also been proposed to be a potential target for tumor immunotherapy. It has been shown to express on tumor-associated macrophages and negatively regulate immune response in tumor.[8] The expression of LILRB4 on monocytic myeloid leukemia cells supports infiltration and inhibits T cell proliferation. Multiple transcript variants encoding different isoforms have been found for this gene.[7]

Interactions

LILRB4 has been shown to interact with PTPN6[9] and INPP5D (SHIP-1).[10]

See also

References

  1. ^ a b c ENSG00000186818, ENSG00000276042, ENSG00000278279, ENSG00000278555 GRCh38: Ensembl release 89: ENSG00000275730, ENSG00000186818, ENSG00000276042, ENSG00000278279, ENSG00000278555 - Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000112023 - Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ Cella M, Döhring C, Samaridis J, Dessing M, Brockhaus M, Lanzavecchia A, Colonna M (May 1997). "A novel inhibitory receptor (ILT3) expressed on monocytes, macrophages, and dendritic cells involved in antigen processing". The Journal of Experimental Medicine. 185 (10): 1743–51. doi:10.1084/jem.185.10.1743. PMC 2196312. PMID 9151699.
  6. ^ Samaridis J, Colonna M (March 1997). "Cloning of novel immunoglobulin superfamily receptors expressed on human myeloid and lymphoid cells: structural evidence for new stimulatory and inhibitory pathways". European Journal of Immunology. 27 (3): 660–5. doi:10.1002/eji.1830270313. PMID 9079806. S2CID 2212182.
  7. ^ a b "Entrez Gene: LILRB4 leukocyte immunoglobulin-like receptor, subfamily B (with TM and ITIM domains), member 4".
  8. ^ Sharma N, Atolagbe OT, Ge Z, Allison JP (July 2021). "LILRB4 suppresses immunity in solid tumors and is a potential target for immunotherapy". The Journal of Experimental Medicine. 218 (7). doi:10.1084/jem.20201811. PMC 8117208. PMID 33974041.
  9. ^ Wang LL, Blasioli J, Plas DR, Thomas ML, Yokoyama WM (February 1999). "Specificity of the SH2 domains of SHP-1 in the interaction with the immunoreceptor tyrosine-based inhibitory motif-bearing receptor gp49B". Journal of Immunology. 162 (3): 1318–23. doi:10.4049/jimmunol.162.3.1318. PMID 9973385.
  10. ^ Zurli V, Wimmer G, Cattaneo F, Candi V, Cencini E, Gozzetti A, et al. (November 2017). "Ectopic ILT3 controls BCR-dependent activation of Akt in B-cell chronic lymphocytic leukemia". Blood. 130 (18): 2006–2017. doi:10.1182/blood-2017-03-775858. PMID 28931525.

Further reading

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.


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