par Kapessidou, Panayota 
;Poulin, Lionel ;Dumoutier, L;Goldman, Michel ;Renauld, J-C;Braun, Michel Y
Référence Transplantation proceedings, 40, 5, page (1593-1597)
Publication Publié, 2008-06
;Poulin, Lionel ;Dumoutier, L;Goldman, Michel ;Renauld, J-C;Braun, Michel Y Référence Transplantation proceedings, 40, 5, page (1593-1597)
Publication Publié, 2008-06
Article révisé par les pairs
| Résumé : | Interleukin-22 (IL-22) was recently described as an effector cytokine produced by TH17 CD4(+) T lymphocytes that, cooperatively with IL-17, mediates IL-23-driven inflammation. Because there was experimental evidence for the role of IL-17 in acute rejection of vascularized allografts, we undertook the present study to assess the function of IL-22 in the process. There was an early transient expression of IL-22 in C57BL/6 mouse cardiac allografts (2-4 days posttransplantation) transplanted to BALB/c recipients. The main source of IL-22 among infiltrating leukocytes was cells expressing the macrophage/monocyte markers Mac3 and CD11b. T cells and granulocytes present in the rejected graft did not express IL-22. Surprisingly, the absence of IL-22 accelerated the rejection of fully histoincompatible hearts. Histology of rejected organs revealed the presence of intensive intragraft thrombosis and disseminated hemorrhagic necrosis. Taken together, these results demonstrated that IL-22 was not an effector lymphokine in cardiac allograft rejection, but early intragraft expression of the cytokine protected it from rejection. |
