A class of immune cells push themselves into an inflammatory state by producing large quantities of a serotonin-making enzyme, according to a study in mice led by scientists at Weill Cornell Medicine.
The study, published March 10 in Immunity, found that the inflammatory and infection-fighting abilities of the cells, called type 2 innate lymphoid cells (ILC2s), are much impaired without the enzyme. The finding suggests possibilities for new treatments targeting ILC2s, which have been linked to asthma and other allergic disorders, to suppress their activation in inflammatory disorders.
The work also hints at what could be a major mechanism of “cross-talk” between the nervous system, which uses serotonin as a signaling molecule or neurotransmitter, and the immune system.
“There’s a lot more to do in terms of understanding the biology of these innate lymphoid cells, but it’s an exciting area that offers us potential new approaches to therapeutic intervention,” said study senior author Dr. David Artis, director of the Jill Roberts Institute for Research in Inflammatory Bowel Disease and the Michael Kors Professor of Immunology in the Department of Medicine at Weill Cornell Medicine.
Read more at Cornell University
Image: The protein interleukin-33 (in green) in the cell nucleus (blue) of stromal cells (red) of mucosal tissue that is embedded in visceral adipose tissue (large octagonal purple cells). CREDIT: Weill Cornell Medicine/Provided