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Macrophages in chronic type 2 inflammation have a novel phenotype characterized by the abundant expression of Ym1 and Fizz1 that can
 

Summary: Macrophages in chronic type 2 inflammation have a novel phenotype
characterized by the abundant expression of Ym1 and Fizz1 that can
be partly replicated in vitro
Meera G. Nair, Daniel W. Cochrane, Judith E. Allen 1
Institute of Cell, Animal and Population Biology, University of Edinburgh, Edinburgh EH9 3JT, UK
Abstract
Using a murine model of nematode infection, we have discovered macrophages that display a novel phenotype that may be
characteristic of macrophages in chronic type 2 inflammation. These nematode-elicited macrophages (NeMf) are characterized by
two unique features: the ability to actively suppress proliferation of a broad range of cell types and the high level expression of two
novel macrophage genes, Ym1 and Fizz1. NeMf also show some similarities with in vitro-derived `alternatively activated
macrophages' such as the downregulation of inflammatory cytokines. We therefore investigated how much of the phenotype
discovered in vivo could be replicated by activation with Th2 cytokines in vitro. Fizz1 and Ym1 were upregulated by IL-4 and IL-13
in vitro but at a considerably lower level than in NeMf. In vitro treatment with IL-4 could also partly replicate the ability of NeMf
to block cellular proliferation. As well as the quantitative differences in gene expression and suppressive phenotype, we also
observed phenotypic differences in the cell morphology between macrophages activated in vivo and in vitro. Although this study
illustrated that macrophages activated in chronic inflammation have distinct features that cannot be readily reproduced in vitro it
also demonstrated that some features of the complex NeMf phenotype can be replicated by treatment of cultured macrophages with
Th2 cytokines. In future, we hope to use in vitro analysis to help define the pathways that lead to this distinctive in vivo macrophage
phenotype.
# 2002 Elsevier Science B.V. All rights reserved.

  

Source: Allen, Judith - School of Biological Sciences, University of Edinburgh

 

Collections: Biology and Medicine