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Notch signaling is emerging as a critical regulator of T cell activation and function. However, there is no reliable cell surface indicator of Notch signaling across activated T cell subsets. In this study, we show that Notch signals induce upregulated expression of the glycosyltransferase gene in T cells mediating graft-versus-host disease after allogeneic bone marrow transplantation in mice. To determine if mediated -glycosylation could be used as a Notch signaling reporter, we quantified the core-2 -glycoform of CD43 in multiple T cell subsets during graft-versus-host disease. Pharmacological blockade of Delta-like Notch ligands abrogated core-2 -glycosylation in a dose-dependent manner after allogeneic bone marrow transplantation, both in donor-derived CD4 and CD8 effector T cells and in Foxp3 regulatory T cells. CD43 core-2 -glycosylation depended on cell-intrinsic canonical Notch signals and identified CD4 and CD8 T cells with high cytokine-producing ability. -deficient T cells still drove lethal alloreactivity, showing that core-2 -glycosylation predicted, but did not cause, Notch-dependent T cell pathogenicity. Using core-2 -glycosylation as a marker of Notch signaling, we identified Ccl19-Cre fibroblastic stromal cells as critical sources of Delta-like ligands in graft-versus-host responses irrespective of conditioning intensity. Core-2 -glycosylation also reported Notch signaling in CD8 T cell responses to dendritic cell immunization, infection, and viral infection. Thus, we uncovered a role for Notch in controlling core-2 -glycosylation and identified a cell surface marker to quantify Notch signals in multiple immunological contexts. Our findings will help refine our understanding of the regulation, cellular source, and timing of Notch signals in T cell immunity.