Alternatively activated macrophages engage in homotypic and heterotypic interactions through IL-4 and polyamine-induced E-cadherin/catenin complexes - PubMed (original) (raw)
. 2009 Nov 19;114(21):4664-74.
doi: 10.1182/blood-2009-05-221598. Epub 2009 Sep 2.
Pieter Bogaert, Jolanda van Hengel, Christopher J Guérin, Geert Berx, Kiavash Movahedi, Rafael Van den Bergh, Anna Pereira-Fernandes, Jan M C Geuns, Hanspeter Pircher, Pierre Dorny, Johan Grooten, Patrick De Baetselier, Jo A Van Ginderachter
Affiliations
- PMID: 19726720
- DOI: 10.1182/blood-2009-05-221598
Free article
Alternatively activated macrophages engage in homotypic and heterotypic interactions through IL-4 and polyamine-induced E-cadherin/catenin complexes
Jan Van den Bossche et al. Blood. 2009.
Free article
Abstract
Alternatively activated macrophages (AAMs), triggered by interleukin-4 (IL-4) and IL-13, play a modulating role during Th2 cytokine-driven pathologies, but their molecular armament remains poorly characterized. Here, we established E-cadherin (Cdh1) as a selective marker for IL-4/IL-13-exposed mouse and human macrophages, which is STAT6-dependently induced during polarized Th2 responses associated with Taenia crassiceps helminth infections or allergic airway inflammation. The IL-4-dependent, arginase-1/ornithine decarboxylase-mediated production of polyamines is important for maximal Cdh1 induction, unveiling a novel mechanism for IL-4-dependent gene transcription. At the macrophage surface, E-cadherin forms a functional complex with the catenins that accumulates at sites of cell contact. Macrophage-specific deletion of the Cdh1 gene illustrates the implication of E-cadherin in IL-4-driven macrophage fusion and heterotypic interactions with CD103(+) and KLRG1(+) T cells. This study identifies the E-cadherin/catenin complex as a discriminative, partly polyamine-regulated feature of IL-4/IL-13-exposed alternatively activated macrophages that contributes to homotypic and heterotypic cellular interactions.
Comment in
- Macrophage fusion cuisine.
Sica A, Mantovani A. Sica A, et al. Blood. 2009 Nov 19;114(21):4609-10. doi: 10.1182/blood-2009-09-242800. Blood. 2009. PMID: 19965712 No abstract available.
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