Abstract:Tissue repair is a subset of a broad repertoire of interleukin-4 (IL-4)- and IL-13-dependent host responses during helminth infection. Here we show that IL-4 or IL-13 alone was not sufficient, but IL-4 or IL-13 together with apoptotic cells induced the tissue repair program in macrophages. Genetic ablation of sensors of apoptotic cells impaired the proliferation of tissue-resident macrophages and the induction of anti-inflammatory and tissue repair genes in the lungs after helminth infection or in the gut afte… Show more
“…IL‐4/13‐dependent macrophage proliferation is enhanced by their production of defense collagens (Minutti et al., 2017), and the types of defense collagens produced are dictated by the tissue location of the macrophages. Making this pro‐inflammatory to anti‐inflammatory switch requires that the macrophages first sense apoptotic neutrophils (Bosurgi et al., 2017). The result is “normal” scar formation, but not regeneration.…”
Section: Formation Of the Accumulation Blastemamentioning
This review explores the historical and current state of our knowledge about urodele limb regeneration. Topics discussed are (1) blastema formation by the proteolytic histolysis of limb tissues to release resident stem cells and mononucleate cells that undergo dedifferentiation, cell cycle entry and accumulation under the apical epidermal cap. (2) The origin, phenotypic memory, and positional memory of blastema cells. (3) The role played by macrophages in the early events of regeneration. (4) The role of neural and AEC factors and interaction between blastema cells in mitosis and distalization. (5) Models of pattern formation based on the results of axial reversal experiments, experiments on the regeneration of half and double half limbs, and experiments using retinoic acid to alter positional identity of blastema cells. (6) Possible mechanisms of distalization during normal and intercalary regeneration. (7) Is pattern formation is a self‐organizing property of the blastema or dictated by chemical signals from adjacent tissues? (8) What is the future for regenerating a human limb?
“…IL‐4/13‐dependent macrophage proliferation is enhanced by their production of defense collagens (Minutti et al., 2017), and the types of defense collagens produced are dictated by the tissue location of the macrophages. Making this pro‐inflammatory to anti‐inflammatory switch requires that the macrophages first sense apoptotic neutrophils (Bosurgi et al., 2017). The result is “normal” scar formation, but not regeneration.…”
Section: Formation Of the Accumulation Blastemamentioning
This review explores the historical and current state of our knowledge about urodele limb regeneration. Topics discussed are (1) blastema formation by the proteolytic histolysis of limb tissues to release resident stem cells and mononucleate cells that undergo dedifferentiation, cell cycle entry and accumulation under the apical epidermal cap. (2) The origin, phenotypic memory, and positional memory of blastema cells. (3) The role played by macrophages in the early events of regeneration. (4) The role of neural and AEC factors and interaction between blastema cells in mitosis and distalization. (5) Models of pattern formation based on the results of axial reversal experiments, experiments on the regeneration of half and double half limbs, and experiments using retinoic acid to alter positional identity of blastema cells. (6) Possible mechanisms of distalization during normal and intercalary regeneration. (7) Is pattern formation is a self‐organizing property of the blastema or dictated by chemical signals from adjacent tissues? (8) What is the future for regenerating a human limb?
“…When damage occurs, inflammatory responses are triggered, which subsequently recruit and activate haematopoietic and non-haematopoietic cells that together orchestrate a cellular response to promote tissue repair [1]. Among the immune cells involved in the response to tissue injury, recent findings have expanded our understanding of repair mechanisms by demonstrating new and unexpected roles for some immune cells in repairing damaged tissue according to organ-specific cues [2-5]. Forkhead box P3‑expressing (Foxp3 + ) regulatory T (Treg) cells are a heterogeneous population that are specializes in antagonizing overexuberant immune responses and restoring immune homeostasis [6].…”
Studies in mice and humans have elucidated an important role for Tregs in promoting tissue repair and restoring tissue integrity. Emerging evidence has revealed that Tregs promoted wound healing and repair processes at multiple tissue sites, such as the heart, liver, kidney, muscle, lung, bone and central nervous system. The localization of repair Tregs in the lung, muscle and liver exhibited unique phenotypes and functions. Epidermal growth factor receptor, amphiregulin, CD73/CD39 and keratinocyte growth factor are important repair factors that are produced or expressed by repair Tregs; these factors coordinate with parenchymal cells to limit injury and promote repair. In addition, repair Tregs can be modulated by IL-33/ST2, TCR signals and other cytokines in the context of injured microenvironment cues. In this review, we provide an overview of the emerging knowledge about Treg-mediated repair in damaged tissues and organs.
“…If macrophages could be aroused for targeted phagocytosis of tumor cells, the energy and substances absorbed by tumor cells may be given back to human body, thus achieving a perfect tumor treatment effect. In addition to phagocytosis, macrophages may also play a role in antigen presenting and in the promotion of inflammatory responses, angiogenesis and tissue healing [58][59][60]. Like other immune cells, macrophages have many types of receptors on their surface, including cytokine receptors, scavenger receptors, TLRs, and Fc receptors [61], which may receive different signals and display different functions.…”
Section: Anti-tumor Strategies For Enhancing Tumor-targeted Phagocytomentioning
The accumulation of mutated somatic cells due to the incompetency of body’s immune system may lead to tumor onset. Therefore, enhancing the ability of the system to eliminate such cells should be the core of tumor therapy. The intrinsic antitumor immunity is triggered by tumor-specific antigens (TSA) or TSA-sensitized dendritic cells (DC). Once initiated, specific anti-tumor antibodies are produced and tumor-specific killer immune cells, including cytotoxic T lymphocytes (CTL), NK cells, and macrophages, are raised or induced. Several strategies may enhance antitumor action of immune system, such as supplying tumor-targeted antibody, activating T cells, enhancing the activity and tumor recognition of NK cells, promoting tumor-targeted phagocytosis of macrophages, and eliminating the immunosuppressive myeloid-derived suppressor cells (MDSCs) and Treg cells. Apart from the immune system, the removal of tumor burden still needs to be assisted by drugs, surgery or radiation. And the body’s internal environment and tumor microenvironment should be improved to recover immune cell function and prevent tumor growth. Multiple microenvironment modulatory therapies may be applied, including addressing hypoxia and oxidative stress, correcting metabolic disorders, and controlling chronic inflammation. Finally, to cure tumor and prevent tumor recurrence, repairing or supporting therapy that consist of tissue repair and nutritional supplement should be applied properly.
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