IMMUNOLOGY2026™ Conference Recordings For Attendees-Defects in CD8+ T cell suppression by Foxp3-dE2 regulatory T cells

Video Transcription

Video Summary

Regulatory T cells (Tregs) maintain immune tolerance, in part through FOXP3, a key transcription factor that exists in humans as two main isoforms: full-length and exon 2–deleted (ΔE2). Individuals expressing only FOXP3 ΔE2 develop severe autoimmunity, suggesting functional defects. Using mouse models engineered to express FOXP3 ΔE2, the study found these Tregs cannot properly suppress CD8 T-cell responses during influenza infection. The defect was intrinsic to ΔE2 Tregs and occurred during the early priming phase of the response. RNA sequencing showed reduced expression of Treg genes such as IL2RA (CD25) and CTLA4, altered chemokine receptor profiles, and reduced IL-2/STAT5 signaling. Experiments confirmed diminished CD25 upregulation, weaker IL-2 “sink” activity, increased IL-2 responsiveness in CD8 T cells, and poorer localization of ΔE2 Tregs to the T-cell zone of lymph nodes. Together, these changes help explain their impaired suppression and link FOXP3 splicing to immune regulation and autoimmunity.

Meta Tag

Date April 17, 2026 1:15 PM - 1:30 PM

Room 156

Session Trouble with the Ex: exTregs and Beyond

Speaker Kristin Weinstein

Track Immune Response Regulation: Cellular Mechanisms (IRC)

Year 2026

Keywords

FOXP3 ΔE2

Regulatory T cells

immune tolerance

CD8 T-cell suppression

autoimmunity

April 17, 2026 1:15 PM - 1:30 PM

156

Trouble with the Ex: exTregs and Beyond

Kristin Weinstein

Immune Response Regulation: Cellular Mechanisms (IRC)

2026