| First Author | Silverman RH | Year | 2002 |
| Journal | Viral Immunol | Volume | 15 |
| Issue | 1 | Pages | 77-83 |
| PubMed ID | 11952148 | Mgi Jnum | J:109855 |
| Mgi Id | MGI:3630031 | Doi | 10.1089/088282402317340242 |
| Citation | Silverman RH, et al. (2002) Skin allograft rejection is suppressed in mice lacking the antiviral enzyme, 2',5'-oligoadenylate-dependent RNase L. Viral Immunol 15(1):77-83 |
| abstractText | The 2-5A/RNase L system is a regulated RNA decay pathway that mediates some of the antiviral and tumor suppressor activities of the interferons. Previously, we demonstrated that RNase L-null mice have increased susceptibility to viral infections and are partially deficient in induced and spontaneous apoptosis. To determine if RNase L functions in cellular, as well as innate, immunity, skin allograft rejection and contact hypersensitivity (CHS) experiments were performed in RNase L+/+ and RNase L-/- mice. Although no consistent alterations in CHS were found, we did observe a delay of 5 days in the acute rejection of class II major histocompatibility complex (MHC) disparate skin allografts in mice lacking RNase L. Accordingly, histologic examinations of the allografts harvested from RNase L-/- mice revealed a dramatic reduction in inflammatory infiltrates, suggesting a delay in T-cell priming or a deficiency in immune cell trafficking. Results consistent with a proinflammatory role for RNase L extend the known functions of the 2-5A/RNase L system beyond innate immunity into some, but not all, types of cellular immunity. |
