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Macrophage galactose‐type C‐type lectins as novel markers for alternatively activated macrophages elicited by parasitic infections and allergic airway inflammation
Author(s) -
Raes Geert,
Brys Lea,
Dahal Bhola K.,
Brandt Jef,
Grooten Johan,
Brombacher Frank,
Vanham Guido,
Noël Wim,
Bogaert Pieter,
Boonefaes Tom,
Kindt Anne,
Van den Bergh Rafaël,
Leenen Pieter J. M.,
De Baetselier Patrick,
Ghassabeh Gholamreza Hassanzadeh
Publication year - 2005
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0304212
Subject(s) - biology , mannose receptor , macrophage , c type lectin , immunology , inflammation , siglec , cytokine , receptor , lectin , in vitro , biochemistry
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.