The Th2 response as monitored by CRTH2 or CCR3 expression is severely decreased during septic shock
The shift of T lymphocytes toward a Th2 profile during septic shock has been established on the basis of in vitro cytokine production. In the present study, the Th2 response was investigated at the level of cell surface marker expression (whole blood flow cytometry). In 58 patients with septic shock...
| Veröffentlicht in: | Clinical immunology (Orlando, Fla.). - 1999. - 113(2004), 3 vom: 12. Dez., Seite 278-84 |
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| 1. Verfasser: | |
| Weitere Verfasser: | , , , , |
| Format: | Aufsatz |
| Sprache: | English |
| Veröffentlicht: |
2004
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| Zugriff auf das übergeordnete Werk: | Clinical immunology (Orlando, Fla.) |
| Schlagworte: | Journal Article Research Support, Non-U.S. Gov't CCR3 protein, human Receptors, CCR3 Receptors, Chemokine Receptors, Immunologic Receptors, Prostaglandin prostaglandin D2 receptor XZF106QU24 |
| Zusammenfassung: | The shift of T lymphocytes toward a Th2 profile during septic shock has been established on the basis of in vitro cytokine production. In the present study, the Th2 response was investigated at the level of cell surface marker expression (whole blood flow cytometry). In 58 patients with septic shock, we observed a reduced CRTH2 (chemoattractant receptor-homologous molecule expressed on Th2 cells) expression on Th2 lymphocytes and regulatory T cells in comparison with 39 healthy volunteers. Eosinophils, which constitutively express CRTH2 in healthy individuals, also exhibited low levels of CRTH2 in patients. In addition, eosinophil CCR3 expression (eotaxin receptor, type 2 chemokine) was strongly correlated with CRTH2, suggesting thus an extended modulation of Th2 related molecules. Importantly, the persistence over time of low levels of CRTH2 or CCR3 expression was found in nonsurvivors. We hypothesize that the restoration of CRTH2/CCR3 expression may be an indicator for optimal recovery after septic shock |
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| Beschreibung: | Date Completed 15.12.2004 Date Revised 30.11.2018 published: Print Citation Status MEDLINE |
| ISSN: | 1521-7035 |