• Gene expression;
  • interferon gamma;
  • microarray;
  • mouse kidney;
  • post-operative injury;
  • rejection

We used Affymetrix Microarrays to define interferon-γ (IFN-γ)-dependent, rejection-induced transcripts (GRITs) in mouse kidney allografts. The algorithm included inducibility by recombinant IFN-γ in kidneys of three normal mouse strains, increase in kidney allografts in three strain combinations and less induction in IFN-γ-deficient allografts. We identified 40 transcripts, which were highly IFN-γ inducible (e.g. Cxcl9, ubiquitin D, MHC), and 168 less sensitive to IFN-γ in normal kidney. In allografts, expression of GRITs was intense and consistent at all time points (day 3 through 42). These transcripts were partially dependent on donor IFN-γ receptors (IFN-γrs): receptor-deficient allografts manifested up to 76% less expression, but some transcripts were highly dependent (ubiquitin D) and others relatively independent (Cxcl9). Kidneys of hosts rejecting allografts showed expression similar to that observed with IFN-γ injections. Many GRITs showed transient IFN-γ-dependent increase in isografts, peaking at day 4–5. GRITs were increased in heart allografts, indicating them as generalized feature of alloresponse. Thus, expression of rejection-induced transcripts is robust and consistent in allografts, reflecting the IFN-γ produced by the alloresponse locally and systemically, acting via host and donor IFN-γr, as well as local IFN-γ production induced by post-operative stress.