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However, the mechanisms by which macrophages participated in pulmonary fibrotic formation were not addressed [ 10]; 2) The enhanced production of IL-8 by the activated monocytes plays an important role.
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Alternatively, macrophages participate in the pro-regenerative capacity of tissue-derived biological scaffolds.
Various cells types including endothelial cells, epithelial cells, activated myofibroblasts and macrophages participate in one or more steps in the fibrotic process [147-149].
It has been shown that macrophage-derived VEGF contributes to angiogenesis and arteriogenesis in ischemic tissues [1], [2], [3], [4] and that the recruitment of macrophages participate in arteriogenesis, blood flow recovery, and angiogenesis [34].
In addition, M2 macrophages participate in tissue repair, angiogenesis, and phagocytosis of apoptotic cells [ 34– 34].
Microglial cells are the resident macrophages participating in the active innate immune defense in the CNS.
Moreover, macrophages participate in the specific immunity as do lymphocytes (Burvenich et al. 2003).
Macrophages participate in an arterial immune-inflammatory reaction triggered by LDL-C [ 22].
In addition, macrophages participate in tissue repair and remodelling, angiogenesis, and restoration of pathogen-disturbed homeostasis [ 4, 7].
Microglia, the brain's resident macrophages, participate in the coordination of events important for the maintenance of neuronal health.
Evidence suggests that several types of leukocytes (mainly B cells, Th17 cells, Th1 cells and macrophages) participate in the immunological attack that produces the lesions [ 29].
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