LILRA5
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesLILRA5, CD85, CD85F, ILT-11, ILT11, LILRB7, LIR-9, LIR9, leukocyte immunoglobulin like receptor A5
External IDsOMIM: 606047 MGI: 3647196 HomoloGene: 83297 GeneCards: LILRA5
Orthologs
SpeciesHumanMouse
Entrez

353514

232801

Ensembl

ENSMUSG00000070873

UniProt

A6NI73

D3Z7A9

RefSeq (mRNA)

NM_181986
NM_021250
NM_181879
NM_181985

NM_001081239

RefSeq (protein)

NP_067073
NP_870994
NP_871714
NP_871715

NP_001074708

Location (UCSC)Chr 19: 54.31 – 54.31 MbChr 7: 4.24 – 4.25 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Leukocyte immunoglobulin-like receptor subfamily A member 5 (LILR-A5) also known as CD85 antigen-like family member F (CD85f), immunoglobulin-like transcript 11 (ILT-11), and leukocyte immunoglobulin-like receptor 9 (LIR-9) is a protein that in humans is encoded by the LILRA5 gene.[5][6][7] This gene is one of the leukocyte receptor genes that form a gene cluster on the chromosomal region 19q13.4.[8] Four alternatively spliced transcript variants encoding distinct isoforms have been described.

Function

The function of LILRA5 is currently unknown. However, it is highly homologous to other LILR genes, thus it is assumed to have similar functions to other LIR family members, i.e. activating and inhibitory functions in leukocytes. Crosslink of this receptor protein on the surface of monocytes has been shown to induce calcium flux and secretion of several proinflammatory cytokines, which suggests the roles of this protein in triggering innate immune responses.[9][10]

Clinical significance

A recent genome-wide association study (GWAS) has found that genetic variations in LILRA5 are associated with late-onset sporadic Alzheimer’s disease (LOAD).[11]

LILBR2 plays a critical role in the inhibition of axonal regeneration and functional recovery after brain injury.[12] However, recent studies demonstrate that LILRB2 is a β-Amyloid receptor and may contribute to synaptic loss and cognitive impairment in Alzheimer's disease.[5][13] Due to its proximity to LILRB2, it is believed that LILRA5 mutation may also contribute to Alzheimer's disease.[11]

References

  1. 1 2 3 ENSG00000274914, ENSG00000275404, ENSG00000187116, ENSG00000278355 GRCh38: Ensembl release 89: ENSG00000274113, ENSG00000274914, ENSG00000275404, ENSG00000187116, ENSG00000278355 - Ensembl, May 2017
  2. 1 2 3 GRCm38: Ensembl release 89: ENSMUSG00000070873 - 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. 1 2 Lao K, Zhang R, Dai Y, Luan J, Guo N, Xu X, et al. (July 2021). "Identification of novel Aβ-LilrB2 inhibitors as potential therapeutic agents for Alzheimer's disease". Molecular and Cellular Neurosciences. 114: 103630. doi:10.1016/j.mcn.2021.103630. PMID 34029694. S2CID 235203153.
  6. ↑ "LILRA5 Gene - Leukocyte Immunoglobulin Like Receptor A5". Gene Cards. Retrieved 2021-12-11.
  7. ↑ "LILRA5 leukocyte immunoglobulin like receptor A5 [Homo sapiens (human)]". Gene - NCBI. National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 2021-12-11.
  8. ↑ Torkar M, Haude A, Milne S, Beck S, Trowsdale J, Wilson MJ (December 2000). "Arrangement of the ILT gene cluster: a common null allele of the ILT6 gene results from a 6.7-kbp deletion". European Journal of Immunology. 30 (12): 3655–3662. doi:10.1002/1521-4141(200012)30:12<3655::AID-IMMU3655>3.0.CO;2-Y. PMID 11169408. S2CID 38450831.
  9. ↑ Mitchell A, Rentero C, Endoh Y, Hsu K, Gaus K, Geczy C, et al. (December 2008). "LILRA5 is expressed by synovial tissue macrophages in rheumatoid arthritis, selectively induces pro-inflammatory cytokines and IL-10 and is regulated by TNF-alpha, IL-10 and IFN-gamma". European Journal of Immunology. 38 (12): 3459–3473. doi:10.1002/eji.200838415. PMID 19009525. S2CID 34746237.
  10. ↑ Truong AD, Hong Y, Nguyen HT, Nguyen CT, Chu NT, Tran HT, et al. (February 2021). "Molecular identification and characterisation of a novel chicken leukocyte immunoglobulin-like receptor A5". British Poultry Science. 62 (1): 68–80. doi:10.1080/00071668.2020.1812524. PMID 32812773. S2CID 221180491.
  11. 1 2 Wightman DP, Jansen IE, Savage JE, Shadrin AA, Bahrami S, Holland D, et al. (September 2021). "A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer's disease". Nature Genetics. 53 (9): 1276–1282. doi:10.1038/s41588-021-00921-z. hdl:1871.1/61f01aa9-6dc7-4213-be2a-d3fe622db488. PMID 34493870. S2CID 237442349.
  12. ↑ Mi YJ, Chen H, Guo N, Sun MY, Zhao ZH, Gao XC, et al. (2017). "Inhibition of PirB Activity by TAT-PEP Improves Mouse Motor Ability and Cognitive Behavior". Frontiers in Aging Neuroscience. 9: 199. doi:10.3389/fnagi.2017.00199. PMC 5476690. PMID 28676756.
  13. ↑ Kim T, Vidal GS, Djurisic M, William CM, Birnbaum ME, Garcia KC, et al. (September 2013). "Human LilrB2 is a β-amyloid receptor and its murine homolog PirB regulates synaptic plasticity in an Alzheimer's model". Science. 341 (6152): 1399–1404. Bibcode:2013Sci...341.1399K. doi:10.1126/science.1242077. PMC 3853120. PMID 24052308.
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