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However, during most chronic\/persistent inflammatory diseases, this tissue repair mechanism is incorrectly regulated and results in irreversible fibrosis in various organs. Fibrosis that severely affects tissue architecture and can cause organ failure is a major cause of death in developed countries. Organ\u2010recruited lymphoid (mainly T cells) and myeloid cells (eosinophils, basophils, macrophages and <jats:styled-content style=\"fixed-case\">DCs<\/jats:styled-content>) have long been recognized in their participation to the development of fibrosis. In particular, a central role for recruited monocyte\u2010derived macrophages in this excessive connective tissue deposit is more and more appreciated. Moreover, the polarization of monocyte\u2010derived macrophages in classically activated (<jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content><jats:italic>\u03b3<\/jats:italic>\u2010dependent) <jats:styled-content style=\"fixed-case\">M1<\/jats:styled-content> cells or alternatively activated (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20104\/<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201013) <jats:styled-content style=\"fixed-case\">M2<\/jats:styled-content> cells, that mirrors the Th1\/Th2 polarization of T cells, is also documented to contribute differentially to the fibrotic process. Here, we review the current understanding of how myeloid cell subpopulations affect the development of fibrosis in parasite infections. Copyright \u00a9 2012 Pathological Society of Great Britain and Ireland. 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