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{{Infobox_gene}}
{{PBB_Controls
'''HLA-G histocompatibility antigen, class I, G''', also known as human leukocyte antigen G ('''HLA-G'''), is a [[protein]] that in humans is encoded by the ''HLA-G'' [[gene]].<ref name= "entrez"/>
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HLA-G belongs to the [[human leukocyte antigen|HLA]] nonclassical class I heavy chain paralogues. This class I molecule is a heterodimer consisting of a heavy chain and a light chain ([[beta-2 microglobulin]]). The heavy chain is anchored in the membrane. HLA-G is expressed on fetal derived placental cells. The heavy chain is approximately 45 kDa and its gene contains 8 exons. Exon one encodes the leader peptide, exons 2 and 3 encode the alpha1 and alpha2 domain, which both bind the peptide, exon 4 encodes the alpha3 domain, exon 5 encodes the transmembrane region, and exon 6 encodes the cytoplasmic tail.<ref name= "entrez">{{cite web | title = Entrez Gene: HLA-G HLA-G histocompatibility antigen, class I, G| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=3135| accessdate = }}</ref> Exon 7 and 8 are not translated due to a stop codon present in exon 6.<ref>{{Cite journal|last=Castelli|first=Erick C.|last2=Mendes-Junior|first2=Celso T.|last3=Veiga-Castelli|first3=Luciana C.|last4=Roger|first4=Michel|last5=Moreau|first5=Philippe|last6=Donadi|first6=Eduardo A.|date=2011-11-01|title=A Comprehensive Study of Polymorphic Sites along the HLA-G Gene: Implication for Gene Regulation and Evolution|url=http://mbe.oxfordjournals.org/content/28/11/3069|journal=Molecular Biology and Evolution|language=en|volume=28|issue=11|pages=3069–3086|doi=10.1093/molbev/msr138|issn=0737-4038|pmid=21622995}}</ref>
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== Function ==
| update_citations = yes
 
}}
HLA-G may play a role in [[immune tolerance in pregnancy]], being expressed in the [[placenta]] by extravillous trophoblast cells (EVT), while the classical [[MHC class I]] genes ([[HLA-A]] and [[HLA-B]]) are not.<ref name="isbn0-7216-0004-2">{{cite book |author1=Jay Iams |author2=Creasy, Robert K. |author3=Resnik, Robert |author4=Robert Reznik | title = Maternal-fetal medicine | edition = | language = | publisher = W.B. Saunders Co | location = Philadelphia | year = 2004 | origyear = | pages = 31–32 | quote = | isbn = 0-7216-0004-2 | oclc = | doi = | url = | accessdate = }}</ref> As HLA-G was first identified in placenta samples, many studies have evaluated its role in pregnancy disorders, such as preeclampsia and recurrent pregnancy loss.<ref>{{Cite journal|last=Michita|first=Rafael Tomoya|last2=Zambra|first2=Francis Maria Báo|last3=Fraga|first3=Lucas Rosa|last4=Sanseverino|first4=Maria Teresa Vieira|last5=Callegari-Jacques|first5=Sidia Maria|last6=Vianna|first6=Priscila|last7=Chies|first7=José Artur Bogo|title=A tug-of-war between tolerance and rejection – New evidence for 3′UTR HLA-G haplotypes influence in recurrent pregnancy loss|url=http://linkinghub.elsevier.com/retrieve/pii/S0198885916301574|journal=Human Immunology|volume=77|issue=10|pages=892–897|doi=10.1016/j.humimm.2016.07.004}}</ref> its downregulation is related to HLA-A and -B downregulation results in protection from [[cytotoxic T cell]] responses, but would in theory result in a ''missing self'' response by [[natural killer cell]]s. HLA-G is a ligand for NK cell inhibitory receptor [[KIR2DL4]], and therefore expression of this HLA by the trophoblast defends it against NK cell-mediated death.<ref name="pmid20061017">{{cite journal |author=Lash, G, Robson, S, Bulmer, J. |title=Review: Functional role of uterine natural killer (uNK) cells in human early pregnancy decidua |journal=Placenta |volume=31 |issue=S |pages=87–92 |year=2010 |pmid=20061017 |doi=10.1016/j.placenta.2009.12.022}}</ref>
 
However, a large family with several members bearing only "null" HLA-G alleles has been found. None of these homozygous subjects have pregnancy or birth difficulties; nor do they present immunodeficiencies, autoimmune diseases, or tumors.<ref name="pmid9089111">{{cite journal |vauthors=Suárez MB, Morales P, Castro MJ, Fernández V, Varela P, Alvarez M, Martínez-Laso J, Arnaiz-Villena A | title = A new HLA-G allele (HLA-G*0105N) and its distribution in the Spanish population | journal = Immunogenetics | volume = 45 | issue = 6 | pages = 464–5 | year = 1997 | pmid = 9089111 | doi =  10.1007/s002510050235}}</ref><ref name="pmid11034559">{{cite journal |vauthors=Casro MJ, Morales P, Rojo-Amigo R, Martinez-Laso J, Allende L, Varela P, Garcia-Berciano M, Guillen-Perales J, Arnaiz-Villena A | title = Homozygous HLA-G*0105N healthy individuals indicate that membrane-anchored HLA-G1 molecule is not necessary for survival | journal = Tissue Antigens | volume = 56 | issue = 3 | pages = 232–9 |date=September 2000 | pmid = 11034559 | doi =  10.1034/j.1399-0039.2000.560305.x}}</ref> It is striking that this "null" allele (HLA-G*01:05N), while it is quite frequent in some populations, like in Iranians, it is almost absent in some Amerindian populations.<ref name="pmid23261410">{{cite journal |vauthors=Arnaiz-Villena A, Enriquez-de-Salamanca M, Areces C, Alonso-Rubio J, Abd-El-Fatah-Khalil S, Fernandez-Honrado M, Rey D | title = HLA-G(∗)01:05N null allele in Mayans (Guatemala) and Uros (Titikaka Lake, Peru): Evolution and population genetics | journal = Hum. Immunol. | volume = 74 | issue = 4 | pages = 478–82 |date=April 2013 | pmid = 23261410 | doi = 10.1016/j.humimm.2012.12.013 }}</ref> Also, some higher primates do not show all MHC-G isoforms.<ref name="pmid11137222">{{cite journal |vauthors=Castro MJ, Morales P, Martinez-Laso J, Allende L, Rojo-Amigo R, Gonzalez-Hevilla M, Varela P, Moscoso J, Garcia-Berciano M, Arnaiz-Villena A | title = Lack of MHC-G4 and soluble (G5, G6) isoforms in the higher primates, [[Pongidae]] | journal = Hum. Immunol. | volume = 61 | issue = 11 | pages = 1164–8 |date=November 2000 | pmid = 11137222 | doi =  10.1016/s0198-8859(00)00189-0}}</ref> In addition, Cercopithecinae middle-sized Old World monkeys do not bear full MHC-G molecules since all of these monkeys present stop codons at MHC-G DNA.<ref name="pmid8606053">{{cite journal |vauthors=Castro MJ, Morales P, Fernández-Soria V, Suarez B, Recio MJ, Alvarez M, Martín-Villa M, Arnaiz-Villena A | title = Allelic diversity at the primate Mhc-G locus: exon 3 bears stop codons in all Cercopithecinae sequences | journal = Immunogenetics | volume = 43 | issue = 6 | pages = 327–36 | year = 1996 | pmid = 8606053 | doi = 10.1007/bf02199801 }}</ref> All of these anomalies must be studied.


<!-- The GNF_Protein_box is automatically maintained by Protein Box Bot.  See Template:PBB_Controls to Stop updates. -->
The presence of soluble HLA-G (sHLA-G) in embryos is associated with better [[pregnancy rate]]s. In order to optimize pregnancy rates, there is significant evidence that a morphological scoring system is the best strategy for the selection of embryos.<ref name=Rebmann>{{cite journal |vauthors=Rebmann V, Switala M, Eue I, Grosse-Wilde H |title=Soluble HLA-G is an independent factor for the prediction of pregnancy outcome after ART: a German multi-centre study |journal=Hum Reprod |volume= 25|issue= 7|pages= 1691–8|date=May 2010 |pmid=20488801 |doi=10.1093/humrep/deq120 |url=}}</ref> However, presence of soluble HLA-G might be considered as a second parameter if a choice has to be made between embryos of morphologically equal quality.<ref name=Rebmann/>
{{GNF_Protein_box
| image = PBB_Protein_HLA-G_image.jpg
| image_source = [[Protein_Data_Bank|PDB]] rendering based on 1ydp.
| PDB = {{PDB2|1ydp}}, {{PDB2|2d31}}, {{PDB2|2dyp}}
| Name = HLA-G histocompatibility antigen, class I, G
| HGNCid = 4964
| Symbol = HLA-G
| AltSymbols =; MHC-G
| OMIM = 142871
| ECnumber =
| Homologene = 83263
| MGIid = 95936
| GeneAtlas_image1 = PBB_GE_HLA-G_211528_x_at_tn.png
| GeneAtlas_image2 = PBB_GE_HLA-G_210514_x_at_tn.png
| GeneAtlas_image3 = PBB_GE_HLA-G_211529_x_at_tn.png
| Function = {{GNF_GO|id=GO:0005515 |text = protein binding}} {{GNF_GO|id=GO:0032393 |text = MHC class I receptor activity}}
| Component = {{GNF_GO|id=GO:0005575 |text = cellular_component}} {{GNF_GO|id=GO:0016020 |text = membrane}} {{GNF_GO|id=GO:0016021 |text = integral to membrane}} {{GNF_GO|id=GO:0042612 |text = MHC class I protein complex}}
| Process = {{GNF_GO|id=GO:0002474 |text = antigen processing and presentation of peptide antigen via MHC class I}} {{GNF_GO|id=GO:0006955 |text = immune response}} {{GNF_GO|id=GO:0006968 |text = cellular defense response}} {{GNF_GO|id=GO:0019882 |text = antigen processing and presentation}}
| Orthologs = {{GNF_Ortholog_box
    | Hs_EntrezGene = 3135
    | Hs_Ensembl = ENSG00000206443
    | Hs_RefseqProtein = NP_002118
    | Hs_RefseqmRNA = NM_002127
    | Hs_GenLoc_db = 
    | Hs_GenLoc_chr = c6_COX
    | Hs_GenLoc_start = 29935685
    | Hs_GenLoc_end = 29939835
    | Hs_Uniprot = P17693
    | Mm_EntrezGene = 15018
    | Mm_Ensembl = 
    | Mm_RefseqmRNA = XM_001004111
    | Mm_RefseqProtein = XP_001004111
    | Mm_GenLoc_db = 
    | Mm_GenLoc_chr = 
    | Mm_GenLoc_start = 
    | Mm_GenLoc_end = 
    | Mm_Uniprot = 
  }}
}}
'''HLA-G histocompatibility antigen, class I, G''', also known as '''HLA-G''', or Human Leukocyte Antigen G, is a human [[gene]].


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==Interactions==
{{PBB_Summary
HLA-G has been shown to [[Protein-protein interaction|interact]] with [[CD8A]].<ref name="pmid10809759">{{cite journal |vauthors=Gao GF, Willcox BE, Wyer JR, Boulter JM, O'Callaghan CA, Maenaka K, Stuart DI, Jones EY, Van Der Merwe PA, Bell JI, Jakobsen BK | title = Classical and nonclassical class I major histocompatibility complex molecules exhibit subtle conformational differences that affect binding to CD8alphaalpha | journal = J. Biol. Chem. | volume = 275 | issue = 20 | pages = 15232–8 |date=May 2000 | pmid = 10809759 | doi = 10.1074/jbc.275.20.15232| url =  }}</ref><ref name="pmid1908512">{{cite journal |vauthors=Sanders SK, Giblin PA, Kavathas P | title = Cell-cell adhesion mediated by CD8 and human histocompatibility leukocyte antigen G, a nonclassical major histocompatibility complex class 1 molecule on cytotrophoblasts | journal = J. Exp. Med. | volume = 174 | issue = 3 | pages = 737–40 |date=September 1991 | pmid = 1908512 | pmc = 2118947 | doi = 10.1084/jem.174.3.737| url = }}</ref>
| section_title =  
| summary_text = HLA-G belongs to the HLA nonclassical class I heavy chain paralogues. This class I molecule is a heterodimer consisting of a heavy chain and a light chain (beta-2 microglobulin). The heavy chain is anchored in the membrane. HLA-G is expressed on fetal derived placental cells. The heavy chain is approximately 45 kDa and its gene contains 8 exons. Exon one encodes the leader peptide, exons 2 and 3 encode the alpha1 and alpha2 domain, which both bind the peptide, exon 4 encodes the alpha3 domain, exon 5 encodes the transmembrane region, and exon 6 encodes the cytoplasmic tail.<ref>{{cite web | title = Entrez Gene: HLA-G HLA-G histocompatibility antigen, class I, G| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=3135| accessdate = }}</ref>
}}


==References==
==References==
{{reflist|2}}
{{reflist}}
 
==Further reading==
==Further reading==
{{refbegin | 2}}
{{refbegin | 2}}
{{PBB_Further_reading
*{{cite journal  |vauthors=Carosella ED, Favier B, Rouas-Freiss N, Moreau P, LeMaoult J |title=Beyond the increasing complexity of the immunomodulatory HLA-G molecule |journal=Blood |volume=111 |issue= 10 |pages= 4862–70 |year= 2008 |pmid= 18334671 |doi=10.1182/blood-2007-12-127662 }}
| citations =
*{{cite journal  |vauthors=Carosella ED, Moreau P, LeMaoult J, Rouas-Freiss N |title=HLA-G: From biology to clinical benefits |journal=Trends in Immunology |volume=29 |issue= 3|pages= 125–32 |year= 2008 |pmid= 18249584 |doi=10.1016/j.it.2007.11.005 }}
*{{cite journal  | author=Arnaiz-Villena A, Martinez-Laso J, Alvarez M, ''et al.'' |title=Primate Mhc-E and -G alleles. |journal=Immunogenetics |volume=46 |issue= 4 |pages= 251-66 |year= 1997 |pmid= 9218527 |doi= }}
{{PBB_Further_reading | citations =
*{{cite journal  | author=Le Bouteiller P |title=HLA-G in the human placenta: expression and potential functions. |journal=Biochem. Soc. Trans. |volume=28 |issue= 2 |pages= 208-12 |year= 2000 |pmid= 10816129 |doi= }}
*{{cite journal  | author=Arnaiz-Villena A |title=Primate Mhc-E and -G alleles |journal=Immunogenetics |volume=46 |issue= 4 |pages= 251–66 |year= 1997 |pmid= 9218527 |doi=10.1007/s002510050271  |name-list-format=vanc| author2=Martinez-Laso J  | author3=Alvarez M  | display-authors=3  | last4=Castro  | first4=Maria J. | last5=Varela  | first5=Pilar  | last6=Gomez-Casado  | first6=Eduardo  | last7=Suarez  | first7=Belen  | last8=Recio  | first8=Mar&#x000ED;a Jos&#x000E9;  | last9=Vargas-Alarc&#x000f3;n  | first9=Gilberto }}
*{{cite journal  | author=Geyer M, Fackler OT, Peterlin BM |title=Structure--function relationships in HIV-1 Nef. |journal=EMBO Rep. |volume=2 |issue= 7 |pages= 580-5 |year= 2001 |pmid= 11463741 |doi= 10.1093/embo-reports/kve141 }}
*{{cite journal  | author=Le Bouteiller P |title=HLA-G in the human placenta: expression and potential functions |journal=Biochem. Soc. Trans. |volume=28 |issue= 2 |pages= 208–12 |year= 2000 |pmid= 10816129 |doi=  }}
*{{cite journal  | author=Langat DK, Hunt JS |title=Do nonhuman primates comprise appropriate experimental models for studying the function of human leukocyte antigen-G? |journal=Biol. Reprod. |volume=67 |issue= 5 |pages= 1367-74 |year= 2003 |pmid= 12390864 |doi=  }}
*{{cite journal  |vauthors=Geyer M, Fackler OT, Peterlin BM |title=Structure–function relationships in HIV-1 Nef |journal=EMBO Rep. |volume=2 |issue= 7 |pages= 580–5 |year= 2001 |pmid= 11463741 |doi= 10.1093/embo-reports/kve141 | pmc=1083955 }}
*{{cite journal  | author=Moreau P, Dausset J, Carosella ED, Rouas-Freiss N |title=Viewpoint on the functionality of the human leukocyte antigen-G null allele at the fetal-maternal interface. |journal=Biol. Reprod. |volume=67 |issue= 5 |pages= 1375-8 |year= 2003 |pmid= 12390865 |doi=  }}
*{{cite journal  |vauthors=Langat DK, Hunt JS |title=Do nonhuman primates comprise appropriate experimental models for studying the function of human leukocyte antigen-G? |journal=Biol. Reprod. |volume=67 |issue= 5 |pages= 1367–74 |year= 2003 |pmid= 12390864 |doi=10.1095/biolreprod.102.005587 }}
*{{cite journal  | author=Moreau P, Rousseau P, Rouas-Freiss N, ''et al.'' |title=HLA-G protein processing and transport to the cell surface. |journal=Cell. Mol. Life Sci. |volume=59 |issue= 9 |pages= 1460-6 |year= 2002 |pmid= 12440768 |doi=  }}
*{{cite journal  |vauthors=Moreau P, Dausset J, Carosella ED, Rouas-Freiss N |title=Viewpoint on the functionality of the human leukocyte antigen-G null allele at the fetal-maternal interface |journal=Biol. Reprod. |volume=67 |issue= 5 |pages= 1375–8 |year= 2003 |pmid= 12390865 |doi=10.1095/biolreprod.102.005439 }}
*{{cite journal  | author=Greenway AL, Holloway G, McPhee DA, ''et al.'' |title=HIV-1 Nef control of cell signalling molecules: multiple strategies to promote virus replication. |journal=J. Biosci. |volume=28 |issue= 3 |pages= 323-35 |year= 2004 |pmid= 12734410 |doi=  }}
*{{cite journal  | author=Moreau P |title=HLA-G protein processing and transport to the cell surface |journal=Cell. Mol. Life Sci. |volume=59 |issue= 9 |pages= 1460–6 |year= 2002 |pmid= 12440768 |doi=10.1007/s00018-002-8521-8 |name-list-format=vanc| author2=Rousseau P  | author3=Rouas-Freiss N  | display-authors=3  | last4=Le Discorde  | first4=M.  | last5=Dausset  | first5=J.  | last6=Carosella  | first6=E. D. }}
*{{cite journal  | author=Bénichou S, Benmerah A |title=[The HIV nef and the Kaposi-sarcoma-associated virus K3/K5 proteins: "parasites"of the endocytosis pathway] |journal=Med Sci (Paris) |volume=19 |issue= 1 |pages= 100-6 |year= 2003 |pmid= 12836198 |doi=  }}
*{{cite journal  | author=Greenway AL |title=HIV-1 Nef control of cell signalling molecules: multiple strategies to promote virus replication |journal=J. Biosci. |volume=28 |issue= 3 |pages= 323–35 |year= 2004 |pmid= 12734410 |doi=10.1007/BF02970151 |name-list-format=vanc| author2=Holloway G  | author3=McPhee DA  | display-authors=3  | last4=Ellis  | first4=Phoebe  | last5=Cornall  | first5=Alyssa  | last6=Lidman  | first6=Michael  }}
*{{cite journal  | author=Le Bouteiller P, Legrand-Abravanel F, Solier C |title=Soluble HLA-G1 at the materno-foetal interface--a review. |journal=Placenta |volume=24 Suppl A |issue= |pages= S10-5 |year= 2004 |pmid= 12842408 |doi= }}
*{{cite journal  |vauthors=Bénichou S, Benmerah A |title=[The HIV nef and the Kaposi-sarcoma-associated virus K3/K5 proteins: "parasites"of the endocytosis pathway] |journal=Med Sci (Paris) |volume=19 |issue= 1 |pages= 100–6 |year= 2003 |pmid= 12836198 |doi=  10.1051/medsci/2003191100}}
*{{cite journal | author=Sköld M, Behar SM |title=Role of CD1d-restricted NKT cells in microbial immunity. |journal=Infect. Immun. |volume=71 |issue= 10 |pages= 5447-55 |year= 2003 |pmid= 14500461 |doi=  }}
*{{cite journal  |vauthors=Le Bouteiller P, Legrand-Abravanel F, Solier C |title=Soluble HLA-G1 at the materno-foetal interface--a review |journal=Placenta |volume=24 Suppl A |issue= |pages= S10–5 |year= 2004 |pmid= 12842408 |doi=10.1053/plac.2002.0931  }}
*{{cite journal  | author=Wiendl H, Mitsdoerffer M, Weller M |title=Express and protect yourself: the potential role of HLA-G on muscle cells and in inflammatory myopathies. |journal=Hum. Immunol. |volume=64 |issue= 11 |pages= 1050-6 |year= 2004 |pmid= 14602235 |doi=  }}
*{{cite journal  |vauthors=Sköld M, Behar SM |title=Role of CD1d-Restricted NKT Cells in Microbial Immunity |journal=Infect. Immun. |volume=71 |issue= 10 |pages= 5447–55 |year= 2003 |pmid= 14500461 |doi=10.1128/IAI.71.10.5447-5455.2003  | pmc=201095  }}
*{{cite journal  | author=Urosevic M, Dummer R |title=HLA-G in skin cancer: a wolf in sheep's clothing? |journal=Hum. Immunol. |volume=64 |issue= 11 |pages= 1073-80 |year= 2004 |pmid= 14602238 |doi=  }}
*{{cite journal  |vauthors=Wiendl H, Mitsdoerffer M, Weller M |title=Express and protect yourself: the potential role of HLA-G on muscle cells and in inflammatory myopathies |journal=Hum. Immunol. |volume=64 |issue= 11 |pages= 1050–6 |year= 2004 |pmid= 14602235 |doi=10.1016/j.humimm.2003.07.001 }}
*{{cite journal  | author=Carosella ED, Moreau P, Le Maoult J, ''et al.'' |title=HLA-G molecules: from maternal-fetal tolerance to tissue acceptance. |journal=Adv. Immunol. |volume=81 |issue= |pages= 199-252 |year= 2004 |pmid= 14711057 |doi=  }}
*{{cite journal  |vauthors=Urosevic M, Dummer R |title=HLA-G in skin cancer: a wolf in sheep's clothing? |journal=Hum. Immunol. |volume=64 |issue= 11 |pages= 1073–80 |year= 2004 |pmid= 14602238 |doi=10.1016/j.humimm.2003.08.351  }}
*{{cite journal  | author=Leavitt SA, SchOn A, Klein JC, ''et al.'' |title=Interactions of HIV-1 proteins gp120 and Nef with cellular partners define a novel allosteric paradigm. |journal=Curr. Protein Pept. Sci. |volume=5 |issue= 1 |pages= 1-8 |year= 2004 |pmid= 14965316 |doi= }}
*{{cite journal  | author=Carosella ED |title=HLA-G molecules: from maternal-fetal tolerance to tissue acceptance |journal=Adv. Immunol. |volume=81 |issue=  |pages= 199–252 |year= 2004 |pmid= 14711057 |doi=10.1016/S0065-2776(03)81006-4  |name-list-format=vanc| author2=Moreau P  | author3=Le Maoult J  | display-authors=3  | series=Advances in Immunology  | last4=Lediscorde  | first4=M  | last5=Dausset  | first5=J  | last6=Rouasfreiss  | first6=N  | isbn=978-0-12-022481-4  }}
*{{cite journal  | author=Le Maoult J, Rouas-Freiss N, Le Discorde M, ''et al.'' |title=[HLA-G in organ transplantation] |journal=Pathol. Biol. |volume=52 |issue= 2 |pages= 97-103 |year= 2004 |pmid= 15001239 |doi= 10.1016/j.patbio.2003.04.006 }}
*{{cite journal  | author=Leavitt SA |title=Interactions of HIV-1 proteins gp120 and Nef with cellular partners define a novel allosteric paradigm |journal=Curr. Protein Pept. Sci. |volume=5 |issue= 1 |pages= 1–8 |year= 2004 |pmid= 14965316 |doi=10.2174/1389203043486955  |name-list-format=vanc| author2=SchOn A  | author3=Klein JC  | display-authors=3  | last4=Manjappara  | first4=Uma  | last5=m. Chaiken  | first5=Irwin  | last6=Freire  | first6=Ernesto  }}
*{{cite journal  | author=Tolstrup M, Ostergaard L, Laursen AL, ''et al.'' |title=HIV/SIV escape from immune surveillance: focus on Nef. |journal=Curr. HIV Res. |volume=2 |issue= 2 |pages= 141-51 |year= 2004 |pmid= 15078178 |doi=  }}
*{{cite journal  | author=Le Maoult J |title=[HLA-G in organ transplantation] |journal=Pathol. Biol. |volume=52 |issue= 2 |pages= 97–103 |year= 2004 |pmid= 15001239 |doi= 10.1016/j.patbio.2003.04.006  |name-list-format=vanc| author2=Rouas-Freiss N  | author3=Le Discorde M  | display-authors=3  | last4=Moreau  | first4=P  | last5=Carosella  | first5=ED }}
*{{cite journal  | author=Joseph AM, Kumar M, Mitra D |title=Nef: "necessary and enforcing factor" in HIV infection. |journal=Curr. HIV Res. |volume=3 |issue= 1 |pages= 87-94 |year= 2005 |pmid= 15638726 |doi= }}
*{{cite journal  | author=Tolstrup M |title=HIV/SIV escape from immune surveillance: focus on Nef |journal=Curr. HIV Res. |volume=2 |issue= 2 |pages= 141–51 |year= 2004 |pmid= 15078178 |doi=10.2174/1570162043484924  |name-list-format=vanc| author2=Ostergaard L  | author3=Laursen AL  | display-authors=3  | last4=Pedersen  | first4=Skou F.  | last5=Duch  | first5=Mogens  }}
*{{cite journal  | author=McIntire RH, Hunt JS |title=Antigen presenting cells and HLA-G--a review. |journal=Placenta |volume=26 Suppl A |issue=  |pages= S104-9 |year= 2005 |pmid= 15837058 |doi= 10.1016/j.placenta.2005.01.006 }}
*{{cite journal  |vauthors=Joseph AM, Kumar M, Mitra D |title=Nef: "necessary and enforcing factor" in HIV infection |journal=Curr. HIV Res. |volume=3 |issue= 1 |pages= 87–94 |year= 2005 |pmid= 15638726 |doi=10.2174/1570162052773013 }}
*{{cite journal  | author=Anderson JL, Hope TJ |title=HIV accessory proteins and surviving the host cell. |journal=Current HIV/AIDS reports |volume=1 |issue= 1 |pages= 47-53 |year= 2005 |pmid= 16091223 |doi=  }}
*{{cite journal  |vauthors=McIntire RH, Hunt JS |title=Antigen presenting cells and HLA-G--a review |journal=Placenta |volume=26 Suppl A |issue=  |pages= S104–9 |year= 2005 |pmid= 15837058 |doi= 10.1016/j.placenta.2005.01.006 }}
*{{cite journal  |vauthors=Anderson JL, Hope TJ |title=HIV accessory proteins and surviving the host cell |journal=Current HIV/AIDS Reports |volume=1 |issue= 1 |pages= 47–53 |year= 2005 |pmid= 16091223 |doi=10.1007/s11904-004-0007-x }}
}}
}}
{{refend}}
{{refend}}
{{PDB Gallery|geneid=3135}}
{{Surface antigens}}


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Latest revision as of 04:02, 3 January 2019

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HLA-G histocompatibility antigen, class I, G, also known as human leukocyte antigen G (HLA-G), is a protein that in humans is encoded by the HLA-G gene.[1]

HLA-G belongs to the HLA nonclassical class I heavy chain paralogues. This class I molecule is a heterodimer consisting of a heavy chain and a light chain (beta-2 microglobulin). The heavy chain is anchored in the membrane. HLA-G is expressed on fetal derived placental cells. The heavy chain is approximately 45 kDa and its gene contains 8 exons. Exon one encodes the leader peptide, exons 2 and 3 encode the alpha1 and alpha2 domain, which both bind the peptide, exon 4 encodes the alpha3 domain, exon 5 encodes the transmembrane region, and exon 6 encodes the cytoplasmic tail.[1] Exon 7 and 8 are not translated due to a stop codon present in exon 6.[2]

Function

HLA-G may play a role in immune tolerance in pregnancy, being expressed in the placenta by extravillous trophoblast cells (EVT), while the classical MHC class I genes (HLA-A and HLA-B) are not.[3] As HLA-G was first identified in placenta samples, many studies have evaluated its role in pregnancy disorders, such as preeclampsia and recurrent pregnancy loss.[4] its downregulation is related to HLA-A and -B downregulation results in protection from cytotoxic T cell responses, but would in theory result in a missing self response by natural killer cells. HLA-G is a ligand for NK cell inhibitory receptor KIR2DL4, and therefore expression of this HLA by the trophoblast defends it against NK cell-mediated death.[5]

However, a large family with several members bearing only "null" HLA-G alleles has been found. None of these homozygous subjects have pregnancy or birth difficulties; nor do they present immunodeficiencies, autoimmune diseases, or tumors.[6][7] It is striking that this "null" allele (HLA-G*01:05N), while it is quite frequent in some populations, like in Iranians, it is almost absent in some Amerindian populations.[8] Also, some higher primates do not show all MHC-G isoforms.[9] In addition, Cercopithecinae middle-sized Old World monkeys do not bear full MHC-G molecules since all of these monkeys present stop codons at MHC-G DNA.[10] All of these anomalies must be studied.

The presence of soluble HLA-G (sHLA-G) in embryos is associated with better pregnancy rates. In order to optimize pregnancy rates, there is significant evidence that a morphological scoring system is the best strategy for the selection of embryos.[11] However, presence of soluble HLA-G might be considered as a second parameter if a choice has to be made between embryos of morphologically equal quality.[11]

Interactions

HLA-G has been shown to interact with CD8A.[12][13]

References

  1. ↑ 1.0 1.1 "Entrez Gene: HLA-G HLA-G histocompatibility antigen, class I, G".
  2. ↑ Castelli, Erick C.; Mendes-Junior, Celso T.; Veiga-Castelli, Luciana C.; Roger, Michel; Moreau, Philippe; Donadi, Eduardo A. (2011-11-01). "A Comprehensive Study of Polymorphic Sites along the HLA-G Gene: Implication for Gene Regulation and Evolution". Molecular Biology and Evolution. 28 (11): 3069–3086. doi:10.1093/molbev/msr138. ISSN 0737-4038. PMID 21622995.
  3. ↑ Jay Iams; Creasy, Robert K.; Resnik, Robert; Robert Reznik (2004). Maternal-fetal medicine. Philadelphia: W.B. Saunders Co. pp. 31–32. ISBN 0-7216-0004-2.
  4. ↑ Michita, Rafael Tomoya; Zambra, Francis Maria Báo; Fraga, Lucas Rosa; Sanseverino, Maria Teresa Vieira; Callegari-Jacques, Sidia Maria; Vianna, Priscila; Chies, José Artur Bogo. "A tug-of-war between tolerance and rejection – New evidence for 3′UTR HLA-G haplotypes influence in recurrent pregnancy loss". Human Immunology. 77 (10): 892–897. doi:10.1016/j.humimm.2016.07.004.
  5. ↑ Lash, G, Robson, S, Bulmer, J. (2010). "Review: Functional role of uterine natural killer (uNK) cells in human early pregnancy decidua". Placenta. 31 (S): 87–92. doi:10.1016/j.placenta.2009.12.022. PMID 20061017.
  6. ↑ Suárez MB, Morales P, Castro MJ, Fernández V, Varela P, Alvarez M, Martínez-Laso J, Arnaiz-Villena A (1997). "A new HLA-G allele (HLA-G*0105N) and its distribution in the Spanish population". Immunogenetics. 45 (6): 464–5. doi:10.1007/s002510050235. PMID 9089111.
  7. ↑ Casro MJ, Morales P, Rojo-Amigo R, Martinez-Laso J, Allende L, Varela P, Garcia-Berciano M, Guillen-Perales J, Arnaiz-Villena A (September 2000). "Homozygous HLA-G*0105N healthy individuals indicate that membrane-anchored HLA-G1 molecule is not necessary for survival". Tissue Antigens. 56 (3): 232–9. doi:10.1034/j.1399-0039.2000.560305.x. PMID 11034559.
  8. ↑ Arnaiz-Villena A, Enriquez-de-Salamanca M, Areces C, Alonso-Rubio J, Abd-El-Fatah-Khalil S, Fernandez-Honrado M, Rey D (April 2013). "HLA-G(∗)01:05N null allele in Mayans (Guatemala) and Uros (Titikaka Lake, Peru): Evolution and population genetics". Hum. Immunol. 74 (4): 478–82. doi:10.1016/j.humimm.2012.12.013. PMID 23261410.
  9. ↑ Castro MJ, Morales P, Martinez-Laso J, Allende L, Rojo-Amigo R, Gonzalez-Hevilla M, Varela P, Moscoso J, Garcia-Berciano M, Arnaiz-Villena A (November 2000). "Lack of MHC-G4 and soluble (G5, G6) isoforms in the higher primates, Pongidae". Hum. Immunol. 61 (11): 1164–8. doi:10.1016/s0198-8859(00)00189-0. PMID 11137222.
  10. ↑ Castro MJ, Morales P, Fernández-Soria V, Suarez B, Recio MJ, Alvarez M, Martín-Villa M, Arnaiz-Villena A (1996). "Allelic diversity at the primate Mhc-G locus: exon 3 bears stop codons in all Cercopithecinae sequences". Immunogenetics. 43 (6): 327–36. doi:10.1007/bf02199801. PMID 8606053.
  11. ↑ 11.0 11.1 Rebmann V, Switala M, Eue I, Grosse-Wilde H (May 2010). "Soluble HLA-G is an independent factor for the prediction of pregnancy outcome after ART: a German multi-centre study". Hum Reprod. 25 (7): 1691–8. doi:10.1093/humrep/deq120. PMID 20488801.
  12. ↑ Gao GF, Willcox BE, Wyer JR, Boulter JM, O'Callaghan CA, Maenaka K, Stuart DI, Jones EY, Van Der Merwe PA, Bell JI, Jakobsen BK (May 2000). "Classical and nonclassical class I major histocompatibility complex molecules exhibit subtle conformational differences that affect binding to CD8alphaalpha". J. Biol. Chem. 275 (20): 15232–8. doi:10.1074/jbc.275.20.15232. PMID 10809759.
  13. ↑ Sanders SK, Giblin PA, Kavathas P (September 1991). "Cell-cell adhesion mediated by CD8 and human histocompatibility leukocyte antigen G, a nonclassical major histocompatibility complex class 1 molecule on cytotrophoblasts". J. Exp. Med. 174 (3): 737–40. doi:10.1084/jem.174.3.737. PMC 2118947. PMID 1908512.

Further reading


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