Systematic review of mouse kidney transplantation

Abstract

A mouse model of kidney transplantation was first described in 1973 by Skoskiewicz et al. Although the mouse model is technically difficult, it is attractive for several reasons: the mouse genome has been characterized and in many aspects is similar to man and there is a greater diversity of experimental reagents and techniques available for mouse studies than other experimental models. We reviewed the literature on all studies of mouse kidney transplantation to report the donor and recipient strain combinations that have been investigated and the resultant survival and histological outcomes. Some models of kidney transplantation have used the transplanted kidney as a life-supporting organ, however, in many studies the recipient mouse's native kidney has been left in situ. Several different combinations of inbred mouse strains have been reported, with varying degrees of injury, survival or tolerance because of haplotype differences. This model has been exceptionally useful as an investigational tool to understand multiple aspects of transplantation including acute rejection, cellular and humoral rejection mechanisms and their treatment. Furthermore, this model has been used to investigate disease mechanisms beyond transplant rejection including intrinsic renal disease and infection-associated pathology.

Targeting Sirtuin-1 prolongs murine renal allograft survival and function

“…In addition, BALB/c to C57BL/6 kidney transplantation is known to elicit less potent rejection than equivalent mismatched heart transplants, which allows longer allograft survival in some of the recipients, and assessment of chronic allograft disease beyond manifestations of early acute cellular rejection and graft loss. 20 …”

Nanoparticle Enhanced MRI Scanning to Detect Cellular Inflammation in Experimental Chronic Renal Allograft Rejection

“…There was a range of values in the allograft group, suggesting a differing amount of inflammation in the different allografts. As the mechanism of rejection in this model of CAD is multifaceted a single measurement at 4 weeks is expected to have variation given that this model develops gradual histological injury up to 12 weeks and beyond [ 38 ].…”

Animal models of kidney inflammation in translational medicine

“…Animals with major-histocompatibility differences require some immunosuppression, which can be used to study drug effects on chronic allograft dysfunction, for example, in dark agoutis into brown-Norway rats treated with an azathioprine, cyclosporine, and steroids [68]. These are just two examples for as many as 28 published combinations of donor and recipient mouse strains published [69]. Strain specific immunological differences as in the ability of CD8+ cells to use alternative modes of costimulation between C57BL/6 and C3H/HeJ mice have to be investigated and recognized in the translational interpretation [70].…”