The trigger for wounds to begin healing may come to this: the interaction of a skin-cell molecule and T-cell molecule, after which damaged skin and the inner surfaces of the gut and lungs begin to repair themselves. The Scripps Research Institute made the discovery, which it hopes could someday lead to targeted treatments for patients such as the elderly or diabetics whose wounds won't heal any longer on their own.
In short, through lab studies with mice, Scripps' research professor Wendy Havran determined that the interaction of the plexin B2 skin-cell receptor and the CD100 receptor found on gamma delta cells is crucial to wound healing, and that cells can't fully begin their healing process if they don't have CD100 in place. In turn, using B2 molecules to stimulate CD100 helped trigger the healing process in T cells and the healing of wounds in mouse intestine linings.
In some ways, this research is incremental, because it helps to understand T cells and how they work, the researchers note. But understanding the mechanism could be crucial to developing new drugs to treat patients whose wounds don't heal well, which means the finding is actually quite significant. Such a drug could stimulate the B2-CD100 interaction, for example, and lead to a targeted vital treatment for patients who could finally embrace a treatment that works to address chronic wounds. Human trials are likely some time away however, so that payoff won't come anytime soon, assuming the results can be repeated in people.
For details, read the latest online issue of the journal Immunity.
- read the release
- check out the journal transcript
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