Key result
Murine ERAP1 deficiency does not impair viral control but is required for antigen cross-presentation.
ERAP1 is required for cross-presentation of cell-associated antigens and immunocomplexes, but its deficiency does not significantly impair in vivo antiviral cytotoxic responses.
Alters selected epitope presentation but preserves most antiviral CTL responses in mice; leaves open ERAP1's necessity for human CTL immunity.
Endoplasmic reticulum-associated aminopeptidase 1 (ERAP1) is involved in the final processing of endogenous peptides presented by MHC class I molecules to CTLs. We generated ERAP1-deficient mice and analyzed cytotoxic responses upon infection with three viruses, including lymphocytic choriomeningitis virus, which causes vigorous T cell activation and is controlled by CTLs. Despite pronounced effects on the presentation of selected epitopes, the in vivo cytotoxic response was altered for only one of several epitopes tested. Moreover, control of lymphocytic choriomeningitis virus was not impaired in the knockout mice. Thus, we conclude that lack of ERAP1 has little influence on antiviral immunohierarchies and antiviral immunity in the infections studied. We also focused on the role of ERAP1 in cross-presentation. We demonstrate that ERAP1 is required for efficient cross-presentation of cell-associated Ag and of OVA/anti-OVA immunocomplexes. Surprisingly, however, ERAP1 deficiency has no effect on cross-presentation of soluble OVA, suggesting that for soluble exogenous proteins, final processing may not take place in an environment containing active ERAP1.
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Firat et al. (2007) studied Viral infection. ERAP1 deficiency vs. Wild-type mice (implied) was evaluated on Cytotoxic responses and viral control. ERAP1 deficiency in mice did not impair the control of lymphocytic choriomeningitis virus and had little influence on antiviral immunity, though it was required for cross-presentation of cell-associated antigens.
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