IMMUNOLOGY2026™ Conference Recordings For Attendees-Mitochondrial DNA oxidation propagates autoimmunity by enabling plasmacytoid dendritic cells to induce TFH differentiation

Mitochondrial DNA oxidation propagates autoimmunity by enabling plasmacytoid dendritic cells to induce TFH differentiation

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Hongshu Xuan presented work showing that stressed mitochondria release oxidized mitochondrial DNA (mtDNA), which can enter circulation and act as a powerful trigger linking inflammation to autoimmunity. In a mouse model using alum-induced sterile inflammation, circulating oxidized mtDNA drove lupus-like disease, including autoantibodies, germinal center expansion, TFH differentiation, kidney damage, and immune infiltration. Single-cell analysis pointed to plasmacytoid dendritic cells (PDCs) as the key sensing cells. In vitro and in vivo, only oxidized—not non-oxidized—mtDNA promoted PDC-dependent TFH responses and autoantibody production. The talk proposed that oxidized mtDNA programs dendritic cells to activate T and B cell responses, helping explain how inflammation transitions into adaptive autoimmunity. Xuan concluded by noting ongoing work on mitochondrial stress in aging, autoimmunity, and neurodegeneration.

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Date April 16, 2026 4:45 PM - 5:00 PM

Room 253

Session Immunometabolism in Autoimmunity

Speaker Hongxu Xian

Track Basic Autoimmunity (BA)

Year 2026

Keywords

oxidized mitochondrial DNA

autoimmunity

plasmacytoid dendritic cells

lupus-like disease

germinal center expansion

TFH differentiation

April 16, 2026 4:45 PM - 5:00 PM

253

Immunometabolism in Autoimmunity

Hongxu Xian

Basic Autoimmunity (BA)

2026