“These findings are very exciting and propel us to look deeper into how the immune system is regulated in the context of health and chronic inflammatory diseases,” said senior investigator Dr.
Furthermore, disrupting this metabolic pathway in mice shuts down pathologic immune responses that would otherwise promote allergic inflammation in the lung.
In this new study, published April 4 in Nature Immunology, Weill Cornell Medicine investigators discovered that inhibiting the activity of an enzyme called Arginase-1 changes the metabolism within ILCs, cutting off a critical nutrient supply. Scientists know from both animal model systems and patient-based studies that a class of immune cells, called innate lymphoid cells (ILCs), play a role in promoting allergic diseases in the lung and other organs. The findings illuminate how nutrients help drive tissue inflammation caused by the immune system – an insight that could lead to new treatments for a wide range of inflammatory conditions from hay fever and food allergies to asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). Starving immune cells of key nutrients stymies their ability to launch an allergic response, according to new research from a multi-institutional collaboration led by Weill Cornell Medicine investigators. A color-enhanced histologic image of allergen-induced type 2 inflammation in mouse lungs.
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