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Important Note: The provided text includes a publication date of January 22, 2026. As of today, February 29, 2024, this research is future research. I will proceed as if the date were current and verify the information as presented, but acknowledge the temporal discrepancy.I will also attempt to find any preliminary reports or related research that might exist now that foreshadows these findings.
How Gut cells Trigger Bone Marrow Responses (Corrected & Verified)
Table of Contents
Dr. Longman’s team found that TL1A is produced mainly by immune cells already present in the inflamed gut of people with IBD. The protein promotes tumor growth primarily by activating ILC3 cells that reside in the intestine. Once activated, these cells release granulocyte-macrophage colony-stimulating factor (GM-CSF), a molecule that stimulates blood cell production.
This signal sets off a process called “emergency granulopoiesis”-a burst of new neutrophil production in bone marrow-followed by the movement of these cells into the gut. In mouse models of intestinal cancer,increasing the number of these neutrophils was shown to accelerate tumor advancement. (Clarified wording – “simply increasing” is less precise)
Tumor-Promoting Changes in Immune Cells
Neutrophils are known to contribute to colorectal cancer by releasing highly reactive molecules that can damage DNA in the cells lining the intestine.The researchers also discovered that ILC3 cells cause neutrophils to adopt a distinct pattern of gene activity. This pattern includes higher expression of genes linked to tumor initiation and growth.
A similar gene activity signature was found in colon tissue samples from patients with IBD-related colitis. Importantly, this tumor-promoting pattern was less pronounced in patients who had received an experimental treatment that blocks TL1A activity.
New Targets for Future Treatments
The findings suggest that several parts of this immune pathway could become targets for future therapies. In addition to TL1A, ILC3 cells, GM-CSF, and the neutrophils recruited by ILC3s may all play roles in new strategies to treat IBD while also reducing the risk of colorectal cancer.
“I think it will be exciting for clinicians in the IBD field to no that there is a systemic process at work here, involving both the gut and the bone marrow, with the potential to drive precision medicine in IBD,” said study first author Dr. Sílvia Pires, an instructor in medicine and member of the Longman Laboratory.
What Comes Next
The research team is continuing to study this immune communication pathway in the context of gut inflammation.Future work will explore whether early or intermittent exposure to GM-CSF may prime bone marrow cells in ways that increase the likelihood of developing IBD over time, possibly opening new avenues for early intervention and prevention.
Reference: “Innate lymphoid cells activated by the cytokine TL1A link colitis to emergency granulopoiesis and the recruitment of tumor-promoting neutrophils” by Sílvia Pires, Wei Yang, Sofia Frigerio, Cynthia Louis, Chloe Scott, Yu Lin Zhou, Emre Cardakli, Nancy tran, Mina Hassan-Zahraee, Zhan Ye, Craig Hyde, kenneth Hung, Amanda Chen, Charles Ng, Alexander Grier, Dana Lukin, Ellen Scherl, Stephan R. Targan, Gretchen E. Diehl, Joep Grootjans, Tracy L. Putoczki, Ian Wicks and Randy S. Longman, 22 January 2026, Immunity. DOI: 10.1016/j.immuni.2025.12.008
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