Fiche publication
Date publication
novembre 2011
Auteurs
Membres identifiés du Cancéropôle Est :
Pr CHALOPIN Jean-Marc
,
Pr DUCLOUX Didier
,
Dr FERRAND Christophe
Tous les auteurs :
Courivaud C, Bamoulid J, Ferrand C, Tiberghien P, Chalopin JM, Saas P, Ducloux D
Lien Pubmed
Résumé
Polyclonal antithymocyte globulins (ATG) induce persistent changes in T-lymphocyte subsets characterized by low CD4 T. The mechanisms remain partly unknown. Prostaglandin E(2) (PGE(2)) is involved in lymphocyte homeostasis. Whether PGE(2) may be involved in persistent CD4 T-cell lymphopenia after ATG is unknown. We examined the association between this polymorphism and CD4 T-cell count in 159 renal transplant recipients (RTR) who received ATG. Analysis of these patients identified 6 CC (3.8%), 32 GC (22.6%), and 117 GG (73.6%) genotypes. Patients with the GG genotype had significantly higher serum PGE(2) concentrations, leading us to compare C carriers with GG patients. Carriers of the C allele had lower CD4 T cell count 1 year (235 +/- 96 vs 323 +/- 227/mm(3); p = 0.022) and 2 years posttransplant (325 +/- 79 vs 422 +/- 231/mm(3); p = 0.024). In multivariate analysis, the C allele (p = 0.029) conferred an increased risk of posttransplant CD4 T-cell lymphocytopenia. Pretransplant T-cell receptor excision circle levels were lower in C carriers. COX-2 gene promoter polymorphism at position -765 (G --> C) is associated with persistent CD4 T-cell lymphopenia after ATG in RTR. This effect is likely to be mediated by the actions of PGE(2) on thymus function and viability.
Référence
Hum Immunol. 2011 Nov;72(11):1060-3
