@article{fdi:010072479,
  title = {{T}he role of {HLA}-{G} in parasitic diseases},
  author = {{S}abbagh, {A}. and {S}onon, {P}. and {S}adissou, {I}. and {M}endes, {C}. {T}. and {G}arcia, {A}ndr{\'e} and {D}onadi, {E}. {A}. and {C}ourtin, {D}avid},
  editor = {},
  language = {{ENG}},
  abstract = {{L}ittle attention has been devoted to the role of {HLA}-{G} gene and molecule on parasitic disorders, and the available studies have focused on malaria, {A}frican and {A}merican trypanosomiasis, leishmaniosis, toxoplasmosis and echinococcosis. {A}fter reporting a brief description regarding the role of the cells of innate and adaptive immune system against parasites, we reviewed the major features of the {HLA}-{G} gene and molecule and the role of {HLA}-{G} on the major cells of immune system. {I}ncreased levels of soluble {HLA}-{G} (s{HLA}-{G}) have been observed in patients presenting toxoplasmosis and in the active phase of echinococcosis. {I}n addition, increased s{HLA}-{G} has also been associated with increased susceptibility to malaria and increased susceptibility to develop human {A}frican trypanosomiasis ({HAT}). {I}n contrast, decreased membrane-bound {HLA}-{G} has been reported in placenta of patients infected with {P}lasmodium falciparum and in heart and colon of patients presenting {C}hagas disease. {T}he 30 untranslated region of the {HLA}-{G} gene has been the main focus of studies on malaria, {HAT} and {C}hagas disease, exhibiting distinct patterns of associations. {C}onsidering that {HLA}-{G} is an immune checkpoint molecule, inhibiting the activity of several cells of the immune system, the excessive neoexpression and the increased s{HLA}-{G} levels together with the decreased constitutive tissue expression of membrane-bound {HLA}-{G} may be detrimental to the host infected with parasite agents.},
  keywords = {echinococcosis ; genetics ; {HLA}-{G} ; immune system ; leishmaniosis ; malaria ; parasite ; toxoplasmosis ; trypanosomiasis ; {AFRIQUE} {SUBSAHARIENNE} ; {AMERIQUE} {LATINE}},
  booktitle = {},
  journal = {{HLA}},
  volume = {91},
  numero = {4},
  pages = {255--270},
  ISSN = {2059-2302},
  year = {2018},
  DOI = {10.1111/tan.13196},
  URL = {https://www.documentation.ird.fr/hor/fdi:010072479},
}