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

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!

LKB1 deficiency in T cells promotes the development of gastrointestinal polyposis T cell–mediated inflammation promotes Peutz–Jeghers syndrome.

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/...

IL-17 links the tumor suppressor LKB1 to gastrointestinal inflammation and polyposis IL-17 is a therapeutic target for intestinal polyposis driven by mutations in the tumor suppressor LKB1.

Happy to post about our latest paper on inflammation and Peutz-Jeghers Syndrome (PJS) in Science Advances. Great work by Dr. Shelby Compton! science.org/doi/10.1126/...

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

Nutrient-driven histone code determines exhausted CD8+ T cell fates Exhausted T cells (TEX) in cancer and chronic viral infections undergo metabolic and epigenetic remodeling, impairing their protective capabilities. However, the impact of nutrient metabolism on epige...

Recent study in @science.org by Allen Distinguished Investigator @drrgjoneslab.bsky.social and collaborators examines the role of histone acetylation in T-cell exhaustion.

www.science.org/doi/10.1126/...