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EGR2 drives TH17 cell pathogenicity in autoimmune neuroinflammation

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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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