“…The SAMP1 strain exhibits a defect in T‐helper cell activity that has not been identified in SAMP8s. Studies in other murine strains indicated that MHC class II activity is reduced in SAMP1 mice (Haruna et al, 1995), MHC class II gene expression is reduced in senescent macrophages where it is not a result of overall impaired responsiveness to IFN‐γ (Herrero et al, 2002), and T lymphocytes from old mice respond less strongly to retroviral superantigen than do those of young mice (Howell et al, 2003). Regardless of the level of IFN‐γ production in the SAMP8s, dysregulation of IFN‐γ production or response in the SAMP‐Os is suggested by the downregulation of many IFN‐γ‐inducible genes in SAMP‐Os, including: the immune factors T‐cell specific GTPase (L38444; Carlow et al, 1998); macrophage‐specific genes allograft inflammatory factor 1 (D86382; Deininger et al, 2002), and monokine induced by γ‐interferon ( MIG ; (M34815; Farber, 1990); macropain ( LMP2 ; D44456), a catalytic subunit of the immunoproteasome that generates immunogenic peptides for presentation by MHC proteins (Goldberg et al, 2002; Yang, 2003); acute phase response factor (U08378; Raz et al, 1994); the antiinflammatory interleukin‐18 binding protein (AB019505; Mühl and Pfeilschifter, 2003); the MHC genes discussed above; the cellular proteins mGBP‐2 (AJ007970; Gorbacheva et al, 2002) and LRG‐47 (U19119; Carlow et al, 1998); and the enzymatic metabolism proteins interferon‐inducible GTPase ( IIGP ; AJ007971; Boehm et al, 1998) and GTPase IGTP (U53219; Taylor et al, 1996).…”