Celiac disease (CeD) is an autoimmune disorder characterized by loss of oral tolerance (LOT) to gluten, with maintenance of a gluten-free diet as the only treatment option. Oral tolerance is mediated by regulatory T cells (Tregs) primed by tolerogenic dendritic cells (DCs). In CeD, there is a breakdown in oral tolerance marked by insufficient gluten-specific Treg responses and expansion of gluten-specific T helper 1 (Th1) cells instead. Environmental triggers such as Type 1 Lang (T1L) reovirus have been found to trigger LOT through pro-inflammatory modulation of CD103+ CD11b- CD8a+ dendritic cells (cDC1s). Our lab has identified that colonization with Tritrichomonas arnold (T.arnold), a novel commensal gut protist, confers protection against T1L-LOT by restraining pro-inflammatory cDC1s. However, the cellular mechanisms driving T.arnold-dependent protection against viral-induced LOT is poorly understood. Recent literature has identified retinoid orphan receptor gamma t (RORgt+) DCs as critical for oral tolerance. These cells are distinct from other DCs for their expression of Prdm16, a transcription factor, and their enrichment in early life. Here, we investigated the role of the RORgt+ DCs in T1L-LOT. Our preliminary data demonstrates that T1L infection induces CD86 expression, a DC activation marker, in vivo. Moreover, T1L infection induces LOT in young mice, despite reported enrichment of RORgt+ DCs. Future studies are underway to determine whether RORgt+ DCs are required for T.arnold-mediated protection. Altogether, our findings highlight RORgt+ DCs as key regulators in T1L-LOT providing insights on the cellular mechanisms maintaining oral tolerance.