|  Help  |  About  |  Contact Us

Publication : Leukocyte-suppressing influences of interleukin (IL)-10 in cardiac allografts: insights from IL-10 knockout mice.

First Author  Räisänen-Sokolowski A Year  1998
Journal  Am J Pathol Volume  153
Issue  5 Pages  1491-500
PubMed ID  9811341 Mgi Jnum  J:50766
Mgi Id  MGI:1309704 Doi  10.1016/S0002-9440(10)65737-9
Citation  Raisanen-Sokolowski A, et al. (1998) Leukocyte-suppressing influences of interleukin (IL)-10 in cardiac allografts: insights from IL-10 knockout mice. Am J Pathol 153(5):1491-500
abstractText  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 a-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.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

3 Bio Entities

0 Expression