Working with human immune cells in the laboratory, Johns Hopkins researchers report they have identified a critical cellular “off” switch for the inflammatory immune response that contributes to lung-constricting asthma attacks. The switch, they say, is composed of regulatory proteins that control an immune signaling pathway in cells. “Asthma patients are constantly firing through this pathway because those proteins are stuck in the ‘on’ position, without proper control by other proteins that shut down this reaction,” says Nicola Heller, PhD, assistant professor of anesthesiology and critical care medicine at the Johns Hopkins University School of Medicine. Asthma has been correlated with an overabundance of one type of immune cell called M2 macrophages in the lungs. In a nonasthmatic person, the M2 macrophages activate to clean up inhaled allergens and foreign particles, and then deactivate when the irritant is broken down. However, in people with asthma, the M2 cells and the chemical signals they emit linger and call in other cells that cause inflammation that can trigger an asthma attack. Over time, the lung is changed by secretions from the M2 cells, which cause the lung tissue to remodel itself, contributing to irreversible obstruction and poor lung function. In the study, Heller’s lab delved deeper into the IRS-2 pathway. By analyzing chemical changes of the IRS-2 protein in immortalized cultures of human white blood cells, it determined that IRS-2 appeared in two different forms — “on,” which allows the signal to pass through, and “off,” which stops the signal from activating the cells into M2 macrophages. Read more Funding: This work was funded by the National Institutes of Health Pathway to Independence Award (K99/R00 HL096897). Raise your voice in support of expanding federal funding for life-saving medical research by joining the AAMC’s advocacy community.
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