Suppression of T-cell functions by human granulocyte arginase

Munder, Markus; Schneider, Henriette; Luckner, Claudia; Giese, Thomas; Langhans, Claus-Dieter; Fuentes, Jose M.; Kropf, Pascale; Mueller, Ingrid; Kolb, Armin; Modolell, Manuel; Ho, Anthony D.

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Suppression of T-cell functions by human granulocyte arginase

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.

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Item Permalink: https://hdl.handle.net/11858/00-001M-0000-002B-9238-A Version Permalink: https://hdl.handle.net/11858/00-001M-0000-002B-9239-8

Genre: Journal Article

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Creators:
Munder, Markus, Author
Schneider, Henriette, Author
Luckner, Claudia, Author
Giese, Thomas, Author
Langhans, Claus-Dieter, Author
Fuentes, Jose M., Author
Kropf, Pascale, Author
Mueller, Ingrid, Author
Kolb, Armin, Author
Modolell, Manuel¹, Author
Ho, Anthony D., Author

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1Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243649

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Abstract: 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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Language(s): eng - English

Dates: Date issued: 2006-09-01

Publication Status: Issued

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Rev. Type: Peer

Identifiers: eDoc: 293655

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Title: Blood

Source Genre: Journal

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Pages: - Volume / Issue: 108 Sequence Number: - Start / End Page: 1627 - 1634 Identifier: -