Sanford-Burnham scientists have identified a potential new way to knock down the inflammation that causes psoriasis, potentially paving the way for new approach to treating the skin condition, according to the Medical Express
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In a study published online in the journal Immunity, the researchers detailed how T cells — key disease-fighting cells that are part of the body's immune system — get fired up to combat threats and then cool down again.
Until now, scientists knew that so-called gamma-delta T-cells were important for initiating inflammatory responses in the skin of people with psoriasis, but not how to turn off these potent cells. The new research identified key factors — known scientifically as B and T Lymphocyte Attenuator (BTLA) inhibitory receptors — that limit inflammatory responses, particularly in the skin.
"Our study shows that BTLA expression in gamma-delta T-cells deactivates their response to immune stimuli," said Carl Ware, professor and director of the Infectious and Inflammatory Disease Center at Sanford-Burnham. "Gamma-delta T-cells are the first line of defense against pathogens — and unless 'turned off,' can lead to unwanted inflammation and tissue destruction."
He said the findings could help scientists develop new treatments for inflammatory disorders by targeting BTLA to reduce inflammation and control disease.
"Understanding the mechanisms that control immune responses creates important breakthroughs for researchers developing drugs to treat these chronic diseases," said Ware.
"If a drug can selectively activate BTLA, we put the brakes on gamma-delta T-cells and gain control of inflammation, prevent damage, and if possible, achieve long-term disease remission."