Abstract
We have presented results that increase our understanding of the roles MC and EOS play in modulating fibrotic processes. In vitro studies have provided clear-cut evidence for the direct involvement of these two inflammatory cells in enhancing proliferation, and either enhancing or decreasing collagen synthesis in human fibroblasts isolated from different anatomical locations. In addition, we have shown that MC and EOS interactions can also take part in modulating fibrosis. In vivo studies in murine and human cGVHD showed that MC activation is detrimental, and that MC stabilization therapy may be helpful in treating the fibrotic outcome of this disease. Much is still obscure. It is, for example, important to define the MC and EOS mediators involved in the modulation of fibroblast properties, and their pattern of influence, keeping in mind the ultimate goal of defining new therapeutic targets for the treatment of fibrotic diseases.
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