UT Southwestern Researchers Find Proteins That Could Help Fight Inflammation and Cancer

Researchers at UT Southwestern have found proteins that help reduce a potentially life-threatening response to chronic infection.

The work may provide a way to control inflammation, which could lead to new medicine and can explain how cancerous cells develop resistance to chemotherapy. When a patient is experiencing chronic inflammation, the immune system can over-respond to something like the flu, causing what is called a cytokine storm, which can be life-threatening. The proteins that were identified help reduce the potentially deadly response.

“This work provides insight into the molecular components required to limit tissue damage associated with uncontrolled inflammation, such as in septic shock, and reveals how cancer cells may suppress the innate immune system during tumor genesis,” said Dr. Neal Alto, Professor of Microbiology at UT Southwestern and the study’s author, via release.

Removing the proteins from those with cancer has made their cancer cells more sensitive new cancer medicines.

“These findings indicate that disruption of this pathway could have important consequences for the pathogenesis of human disease, including cancer,” Alto said via release.

The research was supported by the National Institutes of Health, The Welch Foundation, the Burroughs Wellcome Fund, the Howard Hughes Medical Institute, and the Simons Foundation.

Co-authors include lead author Dr. Zixu Liu, a postdoctoral researcher; graduate student Katrina Mar, former graduate student Dr. Sofya Perelman, and Dr. John Schoggins, Assistant Professor, all of Microbiology. Other co-authors include Dr. Natasha Hanners, an Instructor of Pediatrics; Mohammed Kanchwala of the Eugene McDermott Center for Human Growth and Development; and Dr. Chao Xing, Associate Professor in the McDermott Center and of Bioinformatics and Population and Data Sciences. Dr. Schoggins is a Nancy Cain and Jeffrey A. Marcus Scholar in Medical Research, in Honor of Dr. Bill S. Vowell.

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