Macrophage galactose-type C-type lectins as novel markers for alternatively activated macrophages elicited by parasitic infections and allergic airway inflammation

Molecular markers, especially surface markers associated with type II, cytokine‐dependent, alternatively activated macrophages (aaMF), remain scarce. Besides the earlier documented markers, macrophage mannose receptor and arginase 1, we demonstrated recently that murine aaMF are characterized by inc...

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Published in:Journal of leukocyte biology Vol. 77; no. 3; pp. 321 - 327
Main Authors: Raes, G, Brys, L, Dahal, B K, Brandt, J, Grooten, J, Brombacher, F, Vanham, G, Noel, W, Bogaert, P, Boonefaes, T, Kindt, A, Van den Bergh, R, Leenen, PJM, De Baetselier, P, Ghassabeh, G H
Format: Journal Article
Language:English
Published: United States Society for Leukocyte Biology 01-03-2005
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Summary:Molecular markers, especially surface markers associated with type II, cytokine‐dependent, alternatively activated macrophages (aaMF), remain scarce. Besides the earlier documented markers, macrophage mannose receptor and arginase 1, we demonstrated recently that murine aaMF are characterized by increased expression of found in inflammatory zone 1 (FIZZ1) and the secretory lectin Ym. We now document that expression of the two members of the mouse macrophage galactose‐type C‐type lectin gene family (mMGL1 and mMGL2) is induced in diverse populations of aaMF, including peritoneal macrophages elicited during infection with the protozoan Trypanosoma brucei brucei or the Helminth Taenia crassiceps and alveolar macrophages elicited in a mouse model of allergic asthma. In addition, we demonstrate that in vitro, interleukin‐4 (IL‐4) and IL‐13 up‐regulate mMGL1 and mMGL2 expression and that in vivo, induction of mMGL1 and mMGL2 is dependent on IL‐4 receptor signaling. Moreover, we show that expression of MGL on human monocytes is also up‐regulated by IL‐4. Hence, macrophage galactose‐type C‐type lectins represent novel surface markers for murine and human aaMF.
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ISSN:0741-5400
1938-3673
DOI:10.1189/jlb.0304212