Results from new research conducted at the La Jolla Institute for Allergy & Immunology (LJI) have identified the mechanism by which the protein Sharpin contributes to the regulation of immunosuppressive T cells or Tregs that are essential to the prevention of autoimmune disorders. Previous studies have identified that Sharpin-deficient mice develop inappropriate inflammation, but the new research uncovers that this is due to the absence of a previously unknown cell survival mechanism orchestrated by Sharpin that ensures sufficient Treg populations. This new understanding may illuminate new approaches to the control of immune responses in the treatment of inflammation, autoimmune disorders, or cancer.
In the study, the research team observed an insufficiency of Tregs in the tissue of Sharpin-deficient mice, who developed skin lesions and organ inflammation shortly after birth. The researchers then performed a “rescue” experiment by transferring Tregs from normal mice (mice with intact Sharpin) into mutant mice and observed that the manipulation reduced severity of the inflammation. Study coauthor Hyung-seung Jin, PhD, commented: “Treg-based intervention has in fact been proposed as a novel therapeutic means to treat various inflammatory diseases, meaning that knowing how Treg function is regulated could speed development of effective treatments.”
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The findings are published in the February 1 issue of Nature Immunology. Read more about the findings here.
The article abstract may be read here.