CTLA4-Ig Effectively Controls Clinical Deterioration and Immune Condition in a Murine Model of Foxp3 Deficiency.
Margaux GerbauxEvelyne RoosMathijs WillemsenFrederik StaelsJulika NeumannLeoni BückenJeason HaughtonLidia YshiiJames DooleySusan SchlennerStephanie Humblet-BaronAdrian ListonPublished in: Journal of clinical immunology (2023)
These results highlight the mechanistic diversity of pathogenic pathways initiated by regulatory T cell loss and suggest CTLA4-Ig as a potentially superior therapeutic option for FOXP3-deficient patients.