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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>
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.
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 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/>
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/>
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*{{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  |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  |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=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  }}
*{{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  }}
}}
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Latest revision as of 04:02, 3 January 2019

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez

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Ensembl

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UniProt

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RefSeq (mRNA)

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RefSeq (protein)

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Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
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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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