Suppression of T-cell functions by human granulocyte arginase.

Munder, M; Schneider, H; Luckner, C; Giese, T; Langhans, CD; Fuentes, JM; Kropf, P; Mueller, I; Kolb, A; Modolell, M; Ho, AD; (2006) Suppression of T-cell functions by human granulocyte arginase. Blood, 108 (5). pp. 1627-34. ISSN 0006-4971 DOI:

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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 CD3zeta 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.

Item Type: Article
Faculty and Department: Faculty of Infectious and Tropical Diseases > Dept of Immunology and Infection
PubMed ID: 16709924
Web of Science ID: 240271500036


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