Abstract
BackgroundRegulatory T cells (Treg) protect kidney against ischemia reperfusion (IR) injury via suppressing innate immunity, but the mechanism has not been fully clarified. Soluble fibrinogen-like protein 2 (sFGL2), a novel effector of Treg, may affect apoptosis and inflammation. This study investigated the role of sFGL2 in renal IR injury in a porcine kidney auto-transplantation model.Materials and methodsThe left kidney was retrieved from mini pigs and infused by University of Wisconsin solution into the renal artery with the renal artery and vein clamped for 24-h cold storage. After the right nephrectomy, the left kidney was auto-transplanted into the right for 2 weeks. 3 pigs were sacrificed at day 2, 5, 7, 10 and 14 post-transplantation respectively. Collected renal tissues and daily blood samples were stored for further analyses.ResultsBoth serum creatinine and blood urea nitrogen were maximized during day 2 to 5 and followed by a gradual recovery over 2 weeks. The similar pattern were showed in histological damage, myeloperoxidase + cells and apoptosis in the kidney, as well as circulating TNF-α and IFN-γ. Serum sFGL2 presented a fluctuating increase and reached a peak at day 10. The expression of sFGL2 and its receptor FcγRIIB as well as Foxp3 and IL-10 in the kidney was notably increased from day 5 to 10.ConclusionThe increased sFGL2 together with FcγRIIB during renal recovery after IR injury suggested that sFGL2 might be a potential renoprotective mediator involved in the renal self-repairing and remodeling in this 2-week porcine auto-transplantation model.
Highlights
Kidney transplantation serves as the best treatment for end-stage renal failure patients, many problems related with graft and patient survival have not been solved yet
The increased Soluble fibrinogen-like protein 2 (sFGL2) together with FcγRIIB during renal recovery after ischemia reperfusion (IR) injury suggested that sFGL2 might be a potential renoprotective mediator involved in the renal self-repairing and remodeling in this 2-week porcine auto-transplantation model
The other is sFGL2, the soluble form, constitutively expressed by CD4+ and CD8+ T cells, while Treg cells inducibly secrete it [4]. sFGL2 works as a novel effector of Treg, demonstrating immunoregulatory function to protect against tissue injuries [6]. sFGL2 inhibited dendritic cell maturation and induced B cell apoptosis in vitro, while the downregulation of sFGL2 improved T cell proliferation, promoted Th1 cell polarization and inhibited Treg activity [7]
Summary
Kidney transplantation serves as the best treatment for end-stage renal failure patients, many problems related with graft and patient survival have not been solved yet. IR injury induced inflammation and apoptosis involve in both the innate and adaptive immunity, and jeopardize allograft function eventually. Regulatory T cells (Treg) were shown to protect kidney from IR injury through its immunosuppressive properties in the innate immunity [3], whereas its mechanism has not been fully clarified. One is FGL2 prothrombinase, the membraneprotein form, mainly expressed on the reticuloendothelial cells and exerts procoagulative activity [5]. The other is sFGL2, the soluble form, constitutively expressed by CD4+ and CD8+ T cells, while Treg cells inducibly secrete it [4]. Regulatory T cells (Treg) protect kidney against ischemia reperfusion (IR) injury via suppressing innate immunity, but the mechanism has not been fully clarified. Soluble fibrinogen-like protein 2 (sFGL2), a novel effector of Treg, may affect apoptosis and inflammation. This study investigated the role of sFGL2 in renal IR injury in a porcine kidney auto-transplantation model
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