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Diverse Repertoire of the MHC Class II-Peptide Complexes Is Required for Presentation of Viral Superantigens¹

Tatyana V. Golovkina^2,3,*, Yelena Agafonova^*,, Dmitry Kazansky and Alexander Chervonsky^2,*

^* The Jackson Laboratory, Bar Harbor, ME 04609; and Institute of Carcinogenesis, Cancer Research Center, Moscow, Russia

Among other features, peptides affect MHC class II molecules, causing changes in the binding of bacterial superantigens (b-Sag). Whether peptides can alter binding of viral superantigens (v-Sag) to MHC class II was not known. Here we addressed the question of whether mutations limiting the diversity of peptides bound by the MHC class II molecules influenced the presentation of v-Sag and, subsequently, the life cycle of the mouse mammary tumor virus (MMTV). T cells reactive to v-Sag were found in mice lacking DM molecules as well as in A^bEp-transgenic mice in which MHC class II binding grooves were predominantly occupied by an invariant chain fragment or E^52–68 peptide, respectively. APCs from the mutant mice failed to present v-Sag, as determined by the lack of Sag-specific T cell activation, Sag-induced T cell deletion, and by the aborted MMTV infection. In contrast, mice that express I-A^b with a variety of bound peptides presented v-Sag and were susceptible to MMTV infection. Comparison of v-Sag and b-Sag presentation by the same mutant cells suggested that presentation of v-Sag had requirements similar to that for presentation of toxic shock syndrome toxin-1. Thus, MHC class II peptide repertoire is critical for recognition of v-Sag by the T cells and affects the outcome of infection with a retrovirus.

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