The formation of Foxp3-positive Treg cells occurs in response to any potential allergen, so the findings are applicable to a broad range of allergic reactions and autoimmune diseases, says Dr. de Lafaille. When people suffer from allergies, including life-threatening ones such as asthma, something goes wrong in the process by which Foxp3 signals Treg cell formation. The problem is not necessarily a mutation in the Foxp3 gene, which is known to cause severe autoimmune disease. Rather, something occurs, or fails to occur, in the lungs or the gut that interferes with the production or activity of allergen-specific Treg cells.
The NYU researchers also determined that Treg cells control damage from long-term inflammation. They found high concentrations of Treg cells in inflamed lung tissue of mice without the Foxp3 defect. "The question arose about what these cells are doing in the tissueare they beneficial or not?" Dr. de Lafaille says. It turns out that even though the Treg cells did not prevent inflammation in an ongoing allergic reaction, they kept it under control, ensuring it did not worsen or spread to other areas of the body. "We think that over time these regulatory T cells become more important than the inflammatory cells and end up completely shutting off the inflammation. But it's not overnight and it's not black and white," Dr. de Lafaille emphasizes.
This finding provides a key to one of the most serious consequences of asthma. In addition to breathing problems during an acute attack, people with asthma have chronic inflammation, which can permanently damage their airways. If a means could be found to increase the number of Treg cells in inflamed tissue, this might be prevented. Allergic asthma, the most common and best-u
|Contact: Lorinda Klein|
NYU Langone Medical Center / New York University School of Medicine