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Journal Article

Suppression of T-cell functions by human granulocyte arginase


Modolell,  Manuel
Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Munder, M., Schneider, H., Luckner, C., Giese, T., Langhans, C.-D., Fuentes, J. M., et al. (2006). Suppression of T-cell functions by human granulocyte arginase. Blood, 108, 1627-1634.

Cite as: https://hdl.handle.net/11858/00-001M-0000-002B-9238-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.