Skin Allograft Rejection Is Suppressed in Mice Lacking The Antiviral Enzyme, 2′,5′-Oligoadenylate-Dependent RNase L
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.
Silverman, Robert H.; Zhou, Aimin; Auerbach, Michael B.; Kish, Danielle; Gorbachev, Anton; and Fairchild, Robert L., "Skin Allograft Rejection Is Suppressed in Mice Lacking The Antiviral Enzyme, 2′,5′-Oligoadenylate-Dependent RNase L" (2002). Chemistry Faculty Publications. 445.