Michèlle Rosenzwajg

The paper identifies a shared Treg dysfunction signature across rheumatic diseases, suggesting a therapeutic window of opportunity for Treg-targeted treatments.

This paper develops a third-generation IL-2 therapeutic that targets inflamed tissues via oxidation-specific epitopes, showing improved therapeutic benefit in multiple inflammation models.

This study identifies Treg dysfunction as associated with OA-related pain through multi-omic analysis of peripheral blood from knee OA patients.

This study shows IL-1β signaling affects Tfh and Tfr cells in human lymphoid tissues, linking it to autoantibody production and autoimmune disease.

Maternal immune activation causes Treg deficiency in offspring, leading to brain inflammation and autism-like behaviors, which can be reversed by Treg stimulation.