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drrgjoneslab.bsky.social @drrgjoneslab.bsky.social · 27/06/2025

Hoping that these new insights will lead to new clinical trials and inflammation-targeting therapies for PJS patients!

drrgjoneslab.bsky.social @drrgjoneslab.bsky.social · 27/06/2025

In the current paper we report that LKB1 mutations promote "pathogenic" Th17 responses in the GI tract. Polyps from PJS mice are also enriched with IL-17-producing CD4+, CD8+, and gamma-delta T cells. Treatment of PJS mice with IL-17 blocking antibodies reduces GI polyp growth!

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drrgjoneslab.bsky.social @drrgjoneslab.bsky.social · 27/06/2025

This work builds on our previous unexpected finding that gastrointestinal (GI) polyps found in PJS could be triggered by T cells of the immune system. This work indicated that inflammation by the immune system was a driver of tumor growth in PJS. www.science.org/doi/10.1126/...

science.org

LKB1 deficiency in T cells promotes the development of gastrointestinal polyposis

T cell–mediated inflammation promotes Peutz–Jeghers syndrome.

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Reposted by @drrgjoneslab.bsky.social

Waggoner Lab @labwaggoner.bsky.social · 20/06/2025

IL-17 is a therapeutic target for intestinal polyposis driven by mutations in the tumor suppressor LKB1 www.science.org/doi/10.1126/... @drrgjoneslab.bsky.social

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