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| http://dx.doi.org/10.1016/j.clim.2007.06.006 | DOI Listing |
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Balancing immune response: SHP1 controls neutrophil activation in inflamed lungs.
J Clin Invest
December 2024
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).
View Article and Find Full Text PDFPulmonary arterial hypertension (PAH) is a severe disease caused by progressive distal pulmonary artery obstruction. One cause of PAH are loss-of-function mutations in the potassium channel subfamily K member 3 (KCNK3). KCNK3 encodes a two-pore domain potassium channel, which is crucial for pulmonary circulation homeostasis.
View Article and Find Full Text PDFBLNK negatively regulates innate antifungal immunity through inhibiting c-Cbl-mediated macrophage migration.
Proc Natl Acad Sci U S A
October 2024
Department of Infection and Immunity, Clinical Medicine Scientific and Technical Innovation Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200072, China.
Article Synopsis
- B cell linker protein (BLNK) is essential for signaling in B cells, but its role in macrophages during C-type lectin receptor (CLR) signaling is not well understood.
- The study reveals that CLRs activate BLNK, which hinders macrophage migration by disrupting podosome ring formation in response to fungal components.
- BLNK deficiency leads to increased macrophage migration and enhanced resistance to fungal infections by promoting the recruitment of specific macrophages to affected tissues.
Pseudorabies Virus UL4 protein promotes the ASC-dependent inflammasome activation and pyroptosis to exacerbate inflammation.
PLoS Pathog
September 2024
College of Veterinary Medicine, Northwest A&F University, Yangling, China.
Pseudorabies virus (PRV) infection causes systemic inflammatory responses and inflammatory damages in infected animals, which are associated with the activation of inflammasome and pyroptosis in infected tissues. Here, we identified a critical function of PRV non-structural protein UL4 that enhanced ASC-dependent inflammasome activation to promote pyroptosis. Whereas, the deficiency of viral UL4 was able to reduce ASC-dependent inflammasome activation and the occurrences of pyroptosis.
View Article and Find Full Text PDFA novel role for thioredoxin-related transmembrane protein TMX4 in platelet activation and thrombus formation.
J Thromb Haemost
September 2024
Cyrus Tang Medical Institute, Collaborative Innovation Center of Hematology, State Key Laboratory of Radiation Medicine and Prevention, Soochow University, Suzhou, China. Electronic address:
Background: The functions of critical platelet proteins are controlled by thiol-disulfide exchanges, which are mediated by the protein disulfide isomerase (PDI) family. It has been shown that some PDI family members are important in platelet activation and thrombosis with distinct functions. TMX4, a membrane-type PDI family member, is expressed in platelets, but whether it has a role in platelet activation remains unknown.
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