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Blood, 1 September 2006, Vol. 108, No. 5, pp. 1627-1634. Prepublished online as a Blood First Edition Paper on May 18, 2006; DOI 10.1182/blood-2006-11-010389.
IMMUNOBIOLOGY Suppression of T-cell functions by human granulocyte arginaseFrom the Department of Hematology, Oncology and Rheumatology, University Hospital Heidelberg, Germany; Institute of Immunology, University of Heidelberg, Germany; Children's Hospital, University of Heidelberg, Germany; Departamento de Bioquímica y Biología Molecular, E.U. Enfermería y T.O., Universidad de Extremadura, Cáceres, Spain; Department of Immunology, Faculty of Medicine, Imperial College London, United Kingdom; Department of Surgery, University Hospital Heidelberg, Germany; and Department of Cellular Immunology, Max-Planck-Institute for Immunobiology, Freiburg, Germany.
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 CD3
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| Copyright © 2006 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||||
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. 
