Samantha C. St. Jean

This study shows systemic autoimmunity expands and differentiates microbiota-reactive CD4 T cells, which exacerbate autoimmunity through IL-21 and IFN-gamma mechanisms.

This study shows mutant p53 uses its C-terminal domain to reprogram PARP activity, enabling replication stress adaptation and metastasis in TNBC, and identifies mtp53 as a biomarker for PARP inhibitor and DNA-damaging therapy.

This study shows that loss of the transferrin receptor (CD71) in Treg cells leads to tissue-specific inflammation and autoimmunity, highlighting the role of CD71-iron metabolism in Treg stability and function.