Interleukin-22 deficiency accelerates the rejection of full major histocompatibility complex-disparate heart allografts.
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.
Kapessidou
P
P
Institute for Medical Immunology, Université Libre de Bruxelles (ULB), Gosselies, Belgium.
Poulin
L
L
Dumoutier
L
L
Goldman
M
M
Renauld
J-C
JC
Braun
M Y
MY
D000818:Animals; D005091:Exons; D006084:Graft Rejection / Q000453:epidemiology / Q000276:immunology*; D016027:Heart Transplantation / Q000276:immunology*; D007378:Interleukins / Q000172:deficiency* / Q000235:genetics; D008285:Major Histocompatibility Complex; D051379:Mice; D008807:Mice, Inbred BALB C; D023421:Models, Animal; D014158:Transcription, Genetic; D014184:Transplantation, Homologous; D000097043:Interleukin-22
D007378:Interleukins; D000097043:Interleukin-22