Interleukin-22 deficiency accelerates the rejection of full major histocompatibility complex-disparate heart allografts
(2008) Transplantation Proceedings — Vol. 40, n° 5, p. 1593-1597 (2008)
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- 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.
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Kapessidou, P., Poulin, L., Dumoutier, L., Goldman, M., Renauld, J.-C., & Braun, M. Y. (2008). Interleukin-22 deficiency accelerates the rejection of full major histocompatibility complex-disparate heart allografts. Transplantation Proceedings, 40(5), 1593-1597. https://doi.org/10.1016/j.transproceed.2008.03.151 (Original work published 2008)