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Disturbances in macrophage function can lead to aberrant repair, such that uncontrolled production of in- flammatory mediators and growth factors, deficient generation of anti-inflammatory macrophages, or failed communication between macrophages and epithelial cells, endothelial cells, fibroblasts, and stem or tissue progenitor cells all contribute to a state of persistent injury, and this could lead to the development of path- ological fibrosis.
These molecular triggers induce a complex inflammatory response that is characterized by the recruitment, proliferation, and activation of a variety of hematopoietic and non-hematopoi- etic cells, including neutrophils, macrophages, innate lymphoid cells, natural killer cells, B cells, T cells, fibroblasts, epithelial cells, endothelial cells, and stem cells, which together make up the cellular response that orchestrates tissue repair (Wynn, 2008).
Macrophages produce a variety of factors that stimulate the proliferation, dif- ferentiation, and activation of fibroblasts, epithelial cells, endothelial cells, and stem and progenitor cells that facilitate tissue repair.
epithelial cells
These channels suppress inflammation by transmitting Ca2+ waves to epithelial cells, resulting in the phosphorylation of the pro-survival kinase Akt.
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