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EGR2 drives TH17 cell pathogenicity in autoimmune neuroinflammation

The mechanisms by which TH17 cells can either protect barrier tissues or initiate autoimmunity remain unknown. Here we identify the transcription factor EGR2 as a key determinant of TH17 cell pathogenicity. EGR2 was found to govern TH17 cell migration, regulate the expression of pathogenicity-associated genes, and facilitate the recruitment of other immune cells in the central nervous system.

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Fig. 1: Pathogenic CD4+ T cell responses in MS are associated with upregulation of EGR transcription factors.

References

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This is a summary of: Gao, Y. et al. Transcription factor EGR2 controls homing and pathogenicity of TH17 cells in the central nervous system. Nat. Immunol. https://doi.org/10.1038/s41590-023-01553-7 (2023).

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EGR2 drives TH17 cell pathogenicity in autoimmune neuroinflammation. Nat Immunol 24, 1230–1231 (2023). https://doi.org/10.1038/s41590-023-01568-0

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