Abstract
Abstract Regulatory T cells are not terminally differentiated but can acquire effector properties. Here we report Human Endogenous Retrovirus 1 (HERV1-env) induction of endoplasmic reticulum (ER) stress with Unfolded Protein Response (UPR) activation, through its interaction with ATF6. UPR activation cleaves ATF6 to its α and β isoforms. ATF6α up-regulates RORC, STAT3 and TBX21 and induces IL-17A and INF-γ production in regulatory T cells by binding to promoter sequences. Silencing of HERV1-env results in partial recovery of regulatory T cell suppressive function and abrogation of apoptosis. These findings identify ER stress and UPR activation as key factors driving regulatory T cell plasticity.
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