Recipient Myd88 Deficiency Promotes Spontaneous Resolution of Kidney Allograft Rejection

Journal of the American Society of Nephrology : JASN
Nadine M LerretZheng Zhang

Abstract

The myeloid differentiation protein 88 (MyD88) adapter protein is an important mediator of kidney allograft rejection, yet the precise role of MyD88 signaling in directing the host immune response toward the development of kidney allograft rejection remains unclear. Using a stringent mouse model of allogeneic kidney transplantation, we demonstrated that acute allograft rejection occurred equally in MyD88-sufficient (wild-type [WT]) and MyD88(-/-) recipients. However, MyD88 deficiency resulted in spontaneous diminution of graft infiltrating effector cells, including CD11b(-)Gr-1(+) cells and activated CD8 T cells, as well as subsequent restoration of near-normal renal graft function, leading to long-term kidney allograft acceptance. Compared with T cells from WT recipients, T cells from MyD88(-/-) recipients failed to mount a robust recall response upon donor antigen restimulation in mixed lymphocyte cultures ex vivo. Notably, exogenous IL-6 restored the proliferation rate of T cells, particularly CD8 T cells, from MyD88(-/-) recipients to the proliferation rate of cells from WT recipients. Furthermore, MyD88(-/-) T cells exhibited diminished expression of chemokine receptors, specifically CCR4 and CXCR3, and the impaired abilit...Continue Reading

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Citations

Oct 13, 2016·Transplant International : Official Journal of the European Society for Organ Transplantation·Niina K PalinOlli Ritvos
Dec 13, 2016·Transplantation·Angus W Thomson
Apr 5, 2019·American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons·Zheng ZhangMichael M Abecassis
Aug 11, 2021·Nature Biomedical Engineering·Erika M J SirenJayachandran N Kizhakkedathu

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