Suppression of T-cell functions by human granulocyte arginase
Chronic inflammation is accompanied by impaired T-cell immunity. In the mouse, myeloid cell-associated arginase accounts for the suppression of immune reactivity in various models of tumor growth and chronic infections. Here we show that arginase I is liberated from human granulocytes, and very high...
Gespeichert in:
| Hauptverfasser: | , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
September 1, 2006
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| In: |
Blood
Year: 2006, Jahrgang: 108, Heft: 5, Pages: 1627-1634 |
| ISSN: | 1528-0020 |
| DOI: | 10.1182/blood-2006-11-010389 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1182/blood-2006-11-010389
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| Verfasserangaben: | Markus Munder, Henriette Schneider, Claudia Luckner, Thomas Giese, Claus-Dieter Langhans, Jose M. Fuentes, Pascale Kropf, Ingrid Mueller, Armin Kolb, Manuel Modolell, and Anthony D. Ho |
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| 520 | |a Chronic inflammation is accompanied by impaired T-cell immunity. In the mouse, myeloid cell-associated arginase accounts for the suppression of immune reactivity in various models of tumor growth and chronic infections. Here we show that arginase I is liberated from human granulocytes, and very high activities accumulate extracellularly during purulent inflammatory reactions. Human granulocyte arginase induces a profound suppression of T-cell proliferation and cytokine synthesis. This T-cell phenotype is due to arginase-mediated depletion of arginine in the T-cell environment, which leads to CD3ζ chain down-regulation but does not alter T-cell viability. Our study therefore demonstrates that human granulocytes possess a previously unanticipated immunosuppressive effector function. Human granulocyte arginase is a promising pharmacologic target to reverse unwanted immunosuppression. | ||
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