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PNAS study reveals why organs fail following massive trauma

proteins that carry out bodily functions. Post-traumatic genetic changes had two major effects on T cells: a marked increase in regulatory protein pathways that diminished their function, and a decrease in signals that turn them on, researchers said.

Whether T cells continue to multiply depends on the action of sensitive receptor proteins on their surfaces. Some of the receptors, once activated by signaling molecules, cause the T cell to multiply, while others stop the process or cause the cell to self-destruct. Researchers in the current study identified as many as 20 new receptors on the surfaces of T cells or signaling molecules within T cells, that increase their activity in the case of massive trauma to either cause anergy or apoptosis. Each pathway represents a target for the design of new drugs to reverse T cell shutdown.

The research for the current paper was conducted under the auspices of a Large-Scale Collaborative Award from the National Institute of General Medical Sciences (NIGMS), a division of the National Institutes of Health. Also called "Glue Grants," the awards bring together large teams of researchers to handle extremely complex problems. While the PNAS study patient sample was small, techniques based on it are now being used to study 150 patients per year throughout the Glue grant infrastructure. The glue grant is an open access endeavor as well. The results are posted publicly and hundreds of researchers have already accessed the PNAS study results and applied them to their own projects.

The grant is organized into seven research cores, with the PNAS study written within the Protein Analyses and Cell Biology (PACB) Core working closely with the Genomics Core. PACB include analytical sites, including the one led by Miller-Graziano. She oversaw the separation of white blood cells into pure samples for the PNAS study, and continues to determine cell surface protein expression for the larger Glue grant team.


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Source:University of Rochester Medical Center


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