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However, the induced cell population was not completely characterized, particularly on the protein level.
The proliferation and expansion of neighboring parenchymal and stromal cells are also regulated by macro- phages, and if the injury is severe, macrophages can activate additional stem cell and local progenitor cell populations that participate in repair.
However, at the same time, Kupffer cell death promotes a type 2 response involving the hepatocyte-derived alarmin IL-33 and basophil- derived IL-4, which quickly converts the monocyte-derived macrophages to an M(IL-4)-like phenotype that restores liver ho- meostasis and replenishes the depleted Kupffer cell population.
M(IL-4) cells, in turn, establish an anti-inflammatory environment that is more accommodating to the survival and growth of both MSCs and progenitor populations in injured tissues, suggesting that a mutually beneficial feedback loop exists between anti-in- flammatory macrophages and stem cell populations that drive tissue regeneration (Freytes et al.
Nevertheless, the rapid conversion of these pro- inflammatory TNF-a-producing macrophages to an anti-inflam- matory IL-10- and TGF-b1-producing phenotype appears to be critical to the long-term survival of stem and progenitor cell populations in most tissues (Freytes et al.
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