Skip to Main Content

Within the linings of our guts, immune cells patrol like sentries on a castle wall. These cells, called intraepithelial T lymphocytes, are constantly probing the cells of the gut barrier for signs of disease, killing any cells that appear suspect due to infections or cancer mutations.

A new paper published in Science Immunology on Friday suggests that a subtype of T cells called gamma-delta T cells may be key to that process — and that a protein known as TCF-1 is central to controlling their actions. The work, led by Australian researchers, helps unlock the long underappreciated role of these cells in cancer defense and could open new directions for developing immunotherapies for colorectal cancer, immunologists said.

advertisement

Gamma-delta T cells have been “largely understudied” compared to their immune counterparts, alpha-beta T cells, said Ana Carrizosa Anderson, a cancer researcher at Harvard University who did not work on the study. “This study certainly helps cement the role of gamma-delta T cells in colon malignancy,” she said. “I think it provides a foundation for building understanding of some basic biology or some therapeutic approaches.”

STAT+ Exclusive Story

STAT+

This article is exclusive to STAT+ subscribers

Unlock this article — plus in-depth analysis, newsletters, premium events, and networking platform access.

Already have an account? Log in

Already have an account? Log in

Monthly

$39

Totals $468 per year

$39/month Get Started

Totals $468 per year

Starter

$30

for 3 months, then $39/month

$30 for 3 months Get Started

Then $39/month

Annual

$399

Save 15%

$399/year Get Started

Save 15%

11+ Users

Custom

Savings start at 25%!

Request A Quote Request A Quote

Savings start at 25%!

2-10 Users

$300

Annually per user

$300/year Get Started

$300 Annually per user

View All Plans

Get unlimited access to award-winning journalism and exclusive events.

Subscribe

STAT encourages you to share your voice. We welcome your commentary, criticism, and expertise on our subscriber-only platform, STAT+ Connect

To submit a correction request, please visit our Contact Us page.