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(American Journal of Pathology. 1998;153:1491-1500.)
© 1998 American Society for Investigative Pathology

Regular Articles

Leukocyte-Suppressing Influences of Interleukin (IL)-10 in Cardiac Allografts

Insights from IL-10 Knockout Mice

Anne Räisänen-Sokolowski* , Troels Glysing-Jensen* and Mary E. Russell*{dagger}

From the Cardiovascular Biology Laboratory,* Harvard School of Public Health, and Brigham and Women's Hospital,{dagger} Harvard Medical School, Boston, Massachusetts

To investigate the role of interleukin (IL)-10 in late graft outcomes, we compared BALB/c donor hearts transplanted into immunosuppressed wild-type or IL-10 gene-deficient (-/-) C57BL recipients (n = 49) at 50 ± 5 days. There was prominent leukocyte infiltration and parenchymal destruction with more severe vascular occlusion in grafts from IL-10 -/- recipients. An occlusive CD45+ arteritis with medial necrosis occurred with IL-10 deficiency instead of the {alpha}-smooth muscle actin-rich arteriosclerosis seen in wild-type recipients. Increased interferon (IFN)-{gamma} as well as Mac-1, inducible nitric oxide synthase, and allograft inflammatory factor-1 (but not CD3 and IL-4) transcript levels were seen in allografts from IL-10 -/- recipients as assessed by 32P reverse transcription polymerase chain reaction. We then evaluated the contribution of IFN-{gamma}-mediated responses by neutralizing IFN-{gamma}. Anti-IFN-{gamma} monoclonal antibody (MAb) treatment of IL-10 -/- recipients did not improve graft survival, parenchymal rejection, or occlusive arteritis, indicating that these processes are IFN-{gamma} independent. However, medial smooth muscle cell loss in IL-10 -/- recipients was attenuated by anti-IFN-{gamma} MAb. Hence, in this transplant model, IL-10 suppresses T cell and macrophage responses in the parenchyma and vasculature and confers a protective effect against late rejection.




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