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- W3014458203 abstract "Abstract Background Complement Regulatory Proteins (CRPs), especially CD55 primarily negate complement factor 3-mediated injuries and maintain tissue homeostasis during complement cascade activation. Complement activation and regulation during alloimmune inflammation contribute to allograft injury and therefore we proposed to investigate a crucial pathological link between vascular expression of CD55, active-C3, T cell immunity and associated microvascular tissue injuries during allograft rejection. Methods Balb/c→C57BL/6 allografts were examined for microvascular deposition of CD55, C3d, T cells, and associated tissue microvascular impairments during rejection in mouse orthotopic tracheal transplantation. Results Our findings demonstrated that hypoxia-induced early activation of HIF-1α favors a cell-mediated inflammation (CD4 + , CD8 + , and associated proinflammatory cytokines, IL-2 and TNF-α), which proportionally triggers the downregulation of CRP-CD55, and thereby augments the uncontrolled release of active-C3, and Caspase-3 deposition on CD31 + graft vascular endothelial cells. These molecular changes are pathologically associated with microvascular deterioration (low tissue O 2 and Blood flow) and subsequent airway epithelial injuries of rejecting allografts as compared to non-rejecting syngrafts. Conclusion Together, these findings establish a pathological correlation between complement dysregulation, T cell immunity, and microvascular associated injuries during alloimmune inflammation in transplantation." @default.
- W3014458203 created "2020-04-10" @default.
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- W3014458203 date "2020-03-31" @default.
- W3014458203 modified "2023-10-13" @default.
- W3014458203 title "Hypoxia-induced complement dysregulation is associated with microvascular impairments in mouse tracheal transplants" @default.
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- W3014458203 doi "https://doi.org/10.1186/s12967-020-02305-z" @default.
- W3014458203 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7110829" @default.
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