%0 Journal Article
%9 ACL : Articles dans des revues avec comité de lecture répertoriées par l'AERES
%A Gineau, Laure
%A Courtin, David
%A Camara, M.
%A Ilboudo, H.
%A Jamonneau, Vincent
%A Dias, F. C.
%A Tokplonou, L.
%A Milet, Jacqueline
%A Mendona, P. B.
%A Castelli, E. C.
%A Camara, O.
%A Favier, B.
%A Rouas-Freiss, N.
%A Moreau, P.
%A Donadi, E. A.
%A Bucheton, Bruno
%A Sabbagh, A.
%A Garcia, André
%T Human leukocyte antigen-G : a promising prognostic marker of disease progression to improve the control of human African trypanosomiasis
%D 2016
%L fdi:010068692
%G ENG
%J Clinical Infectious Diseases
%@ 1058-4838
%K HLA-G ; human African trypanosomiasis ; Trypanosoma brucei gambiense ; susceptibility ; genetic association
%K GUINEE
%M ISI:000387986200012
%N 9
%P 1189-1197
%R 10.1093/cid/ciw505
%U https://www.documentation.ird.fr/hor/fdi:010068692
%> https://www.documentation.ird.fr/intranet/publi/2016/12/010068692.pdf
%V 63
%W Horizon (IRD)
%X Background. Human African trypanosomiasis (HAT) caused by Trypanosoma brucei gambiense can be diagnosed in the early hemolymphatic stage (stage 1 [S1]) or meningoencephalitic stage (stage 2 [S2]). Importantly, individuals harbouring high and specific antibody responses to Tbg antigens but negative parasitology are also diagnosed in the field (seropositive [SERO]). Whereas some develop the disease in the months following their initial diagnosis (SERO/HAT), others remain parasitologically negative for long periods (SERO) and are apparently able to control infection. Human leucocyte antigen (HLA)-G, an immunosuppressive molecule, could play a critical role in this variability of progression between infection and disease. Methods. Soluble HLA-G (sHLA-G) was measured in plasma for patients in the SERO (n = 65), SERO/HAT (n = 14), or HAT (n = 268) group and in cerebrospinal fluid for patients in S1 (n = 55), early S2 (n = 93), or late S2 (n = 110). Associations between these different statuses and the soluble level or genetic polymorphisms of HLA-G were explored. Results. Plasma sHLA-G levels were significantly higher in HAT (P = 6 x 10(-7)) and SERO/HAT (P = .007) than SERO patients. No difference was observed between the SERO/HAT and HAT groups. Within the HAT group, specific haplotypes (HG010102 and HG0103) displayed increased frequencies in S1 (P = .013) and late S2 (P = .036), respectively. Conclusions. These results strongly suggest the involvement of HLA-G in HAT disease progression. Importantly, high plasma sHLA-G levels in SERO patients could be predictive of subsequent disease development and could represent a serological marker to help guide therapeutic decision making. Further studies are necessary to assess the predictive nature of HLA-G and to estimate both sensitivity and specificity.
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