6533b7d4fe1ef96bd1261f24

RESEARCH PRODUCT

Thy-1 (CD90) regulates the extravasation of leukocytes during inflammation.

Guido HildebrandtJörg LehmannUlf AndereggTobias PolteUlrike BönischKathleen SchubertSina I. SchaderJan C. SimonRafaela HoltappelsAnja Saalbach

subject

ChemokineMice 129 StrainNeutrophilsmedicine.medical_treatmentT-LymphocytesImmunologyInflammationCD18In Vitro TechniquesPeritonitisMonocytesMiceCell MovementCell AdhesionLeukocytesImmunology and AllergyMedicineAnimalsHumansCD90Thy-1InflammationMice KnockoutTransplantation Chimerabiologybusiness.industryInterleukinsEndothelial CellsPneumoniaExtravasationTransplantationEosinophilsMice Inbred C57BLCytokineIntegrin alpha MImmunologybiology.proteinThy-1 Antigensmedicine.symptomChemokinesbusinessextravasationPeptide Hydrolases

description

Human Thy-1 (CD90) has been shown to mediate adhesion of inflammatory cells to activated microvascular endothelial cells via interaction with Mac-1 (CD11b/CD18) in vitro. Since there are no data showing the physiological relevance of Thy-1 for the recruitment of inflammatory cells in vivo, different inflammation models were investigated in Thy-1-deficient mice and littermate controls. In thioglycollate-induced peritonitis, the number of neutrophils and monocytes was significantly diminished in Thy-1-deficient mice. During acute lung inflammation, the extravasation of eosinophils and monocytes into the lung was significantly reduced in Thy-1-deficient mice. Moreover, during chronic lung inflammation, the influx of eosinophils and monocytes was also strongly decreased. These effects were independent of Thy-1 expression on T cells, as shown by the transplantation of WT BM into the Thy-1-deficient mice. In spite of the strong Thy-1 expression on T cells in the chimeric mice , the extravasation of the inflammatory cells in these mice was significantly diminished, compared to control mice. Finally, the altered number and composition of infiltrating leukocytes in Thy-1-deficient mice modified the chemokine/cytokine and protease expression at the site of inflammation. In conclusion, Thy-1 is involved in the control of inflammatory cell recruitment and, thus, also in conditioning the inflammatory microenvironment.

10.1002/eji.201041117https://pubmed.ncbi.nlm.nih.gov/21264853