Balancing immune response: SHP1 controls neutrophil activation in inflamed lungs.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 39680457.
- Also identified by DOI 10.1172/JCI187056 and PMC identifier 11645135.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Following respiratory infection or injury, neutrophil hyperactivation can damage surrounding lung tissue by releasing harmful compounds. In this issue of the JCI, Moussavi-Harami and colleagues identified tyrosine phosphatase SHP1 as a key negative regulator of neutrophil activation in acute respiratory distress syndrome (ARDS). Neutrophil-specific Shp1 disruption leads to hyperinflammation, pulmonary hemorrhage, and increased mortality in both sterile and pathogen-induced acute lung injury (ALI). Large intravascular neutrophil clusters and excessive PAD4-independent neutrophil extracellular traps (NETs) were identified as key features of lung injury. Mechanistically, Shp1 deficiency resulted in uncontrolled SYK kinase activation, driving chaotic neutrophil hyperactivation and inflammation.
Medical subject headings
- Protein Tyrosine Phosphatase, Non-Receptor Type 6
- Neutrophil Activation
- Neutrophils