Interleukin-9 promotes eosinophilic rejection of mouse heart allografts
(2003) Transplantation — Vol. 76, n° 3, p. 572-577 (2003)
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- Background. Eosinophils participate in allograft rejection when donor-reactive helper T lymphocytes are T-helper type 2 (Th2)-biased. Whereas the involvement of interleukin (IL)-4 and IL-5 in these forms of rejection is well established, the role of IL-9, another Th2-type cytokine promoting eosinophilia, has not been determined. Methods. We first used real-time polymerase chain reaction to quantify IL-9 mRNA in rejected allografts in a mouse model of fully mismatched heart transplantation in which recipients were devoid of CD8 T cells and developed a Th2 alloimmune response. We then compared allograft survival in wild-type versus IL-9-deficient mice depleted of CD8 T cells. Finally, we compared the fate of major histocompatibility complex class II-mismatched cardiac transplants from wild-type versus IL-9 transgenic donors to determine the influence of IL-9 overexpression within the graft. Results. The Th2 alloimmune response in CD8-deficient mice was associated with the accumulation of IL-9 mRNA in the rejected graft. In IL-9-deficient recipients depleted of CD8 T cells, eosinophil infiltration of heart allografts did not develop, but rejection still occurred. In the major histocompatibility complex class 11 disparate model, heart allografts from IL-9 transgenic donors were acutely rejected, whereas grafts from wild-type donors did not develop rejection. Acute rejection of IL-9 transgenic hearts was associated with massive eosinophil infiltration and prevented by neutralization of either IL-4 or IL-5. Conclusion. IL-9 is critically involved in heart transplant eosinophilia in conjunction with IL-4 and IL-5.
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Poulin, L., Richard, M., Le Moine, A., Kiss, R., McKenzie, A., Goldman, M., Renauld, J.-C., Van Snick, J., & Braun, M. (2003). Interleukin-9 promotes eosinophilic rejection of mouse heart allografts. Transplantation, 76(3), 572-577. https://doi.org/10.1097/01.TP.0000071201.32424.D2 (Original work published 2003)