Sabbagh A. auteur aut IRD Sonon P. auteur aut IRD Sadissou I. auteur aut IRD Mendes C. T. auteur aut IRD Garcia André auteur aut IRD Donadi E. A. auteur aut IRD Courtin David auteur aut IRD text journalArticle eng text/pdf born digital access Little attention has been devoted to the role of HLA-G gene and molecule on parasitic disorders, and the available studies have focused on malaria, African and American trypanosomiasis, leishmaniosis, toxoplasmosis and echinococcosis. After 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. Increased levels of soluble HLA-G (sHLA-G) have been observed in patients presenting toxoplasmosis and in the active phase of echinococcosis. In addition, increased sHLA-G has also been associated with increased susceptibility to malaria and increased susceptibility to develop human African trypanosomiasis (HAT). In contrast, decreased membrane-bound HLA-G has been reported in placenta of patients infected with Plasmodium falciparum and in heart and colon of patients presenting Chagas disease. The 30 untranslated region of the HLA-G gene has been the main focus of studies on malaria, HAT and Chagas disease, exhibiting distinct patterns of associations. Considering that HLA-G is an immune checkpoint molecule, inhibiting the activity of several cells of the immune system, the excessive neoexpression and the increased sHLA-G levels together with the decreased constitutive tissue expression of membrane-bound HLA-G may be detrimental to the host infected with parasite agents. specialized echinococcosis genetics HLA-G immune system leishmaniosis malaria parasite toxoplasmosis trypanosomiasis AFRIQUE SUBSAHARIENNE AMERIQUE LATINE 052 050 91 4 255-270 2018 2059-2302 https://www.documentation.ird.fr/hor/fdi:010072479 10.1111/tan.13196 2059-2302 [F B010072479] https://www.documentation.ird.fr/hor/fdi:010072479 https://www.documentation.ird.fr/intranet/publi/2018/04/010072479.pdf Accès réservé (Intranet de l'IRD) IRD - Base Horizon / Pleins textes 2018-05-04 2018-05-04 fdi:010072479 fre