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Journal of Biomedicine and Biotechnology
Volume 2010 (2010), Article ID 683485, 10 pages
Review Article

Arginase in Parasitic Infections: Macrophage Activation, Immunosuppression, and Intracellular Signals

Inmunología, CIBICI-CONICET, Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, 5000 Córdoba, Argentina

Received 31 July 2009; Accepted 30 September 2009

Academic Editor: Luis I. Terrazas

Copyright © 2010 Cinthia C. Stempin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


A type 1 cytokine-dependent proinflammatory response inducing classically activated macrophages (CaM 𝜙 s) is crucial for parasite control during protozoan infections but can also contribute to the development of immunopathological disease symptoms. Type 2 cytokines such as IL-4 and IL-13 antagonize CaM 𝜙 s inducing alternatively activated macrophages (AaM 𝜙 s) that upregulate arginase-1 expression. During several infections, induction of arginase-1-macrophages was showed to have a detrimental role by limiting CaM 𝜙 -dependent parasite clearance and promoting parasite proliferation. Additionally, the role of arginase-1 in T cell suppression has been explored recently. Arginase-1 can also be induced by IL-10 and transforming growth factor- 𝛽 (TGF- 𝛽 ) or even directly by parasites or parasite components. Therefore, generation of alternative activation states of macrophages could limit collateral tissue damage because of excessive type 1 inflammation. However, they affect disease outcome by promoting parasite survival and proliferation. Thus, modulation of macrophage activation may be instrumental in allowing parasite persistence and long-term host survival.