IMMUNOLOGY2026™ Conference Recordings For Attendees-ExTh17 Cells Arising from Th17 Support Chronic RA-Like Inflammation Independent of IL-17

ExTh17 Cells Arising from Th17 Support Chronic RA-Like Inflammation Independent of IL-17

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Video Summary

The speaker presented research on rheumatoid arthritis, focusing on how TH17 cells change into more pathogenic “XTH17” cells during disease progression. Using a new fate-mapping mouse model, they showed that after arthritis develops, TH17 cells lose IL-17 expression and become XTH17 cells, which are more abundant in lymph nodes and joints and drive more severe inflammation, bone, and cartilage damage. Bulk and single-cell analyses identified genes such as S1PR4 and CD44 as important in this transition, with interferon-related genes also enriched. Human rheumatoid arthritis datasets confirmed these markers. Co-culture and imaging experiments showed that fibroblast-like synovial cells promote this conversion, and XTH17 cells localize near fibroblasts in inflamed joints. Knockdown of S1PR4 or CD44 reduced XTH17 abundance and arthritis severity. Overall, the study suggests that XTH17 cells, not IL-17 alone, sustain chronic rheumatoid arthritis and may be a promising therapeutic target.

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Date April 17, 2026 1:45 PM - 2:00 PM

Room 156

Session Trouble with the Ex: exTregs and Beyond

Speaker Martina Zoccheddu

Track Immune Response Regulation: Cellular Mechanisms (IRC)

Year 2026

Keywords

rheumatoid arthritis

TH17 cells

XTH17 cells

S1PR4

CD44

April 17, 2026 1:45 PM - 2:00 PM

156

Trouble with the Ex: exTregs and Beyond

Martina Zoccheddu

Immune Response Regulation: Cellular Mechanisms (IRC)

2026