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.
journal_name
Bloodjournal_title
Bloodauthors
Van den Bossche J,Bogaert P,van Hengel J,Guérin CJ,Berx G,Movahedi K,Van den Bergh R,Pereira-Fernandes A,Geuns JM,Pircher H,Dorny P,Grooten J,De Baetselier P,Van Ginderachter JAdoi
10.1182/blood-2009-05-221598subject
Has Abstractpub_date
2009-11-19 00:00:00pages
4664-74issue
21eissn
0006-4971issn
1528-0020pii
blood-2009-05-221598journal_volume
114pub_type
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