Kidney protection against autoreactive CD8(+) T cells distinct from immunoprivilege and sequestration
- Details
- Publication Year 2001-08,Volume 60,Issue #2,Page 664-671
- Journal Title
- KIDNEY INTERNATIONAL
- Publication Type
- Journal Article
- Abstract
- Background. The kidney tubulointerstitium has been re ported to be protected from T-cell-mediated damage by sequestration from the T-cell compartment. We examined the ability of autoreactive T cells to infiltrate the kidney in a transgenic mouse model. Methods. RIP-mOVA transgenic mice express the model autoantigen. membrane-bound ovalbumin (mOVA). in kidney proximal tubular cells and pancreatic beta cells. OVA-specific CD8+ Tcells (OT-I cells) were transferred into these recipient mice and their immune response against pancreas and kidney tissue was compared. Results. When OVA-specific CD8+ T cells (OT-I cells) were injected into RIP-mOVA mice, they were activated in the renal and pancreatic lymph nodes by cross-presentation, These in vivo-activated OT-I cells caused the destruction of pancreatic islets leading to autoimmune diabetes, but did not infiltrate the kidney. Neither CD95-CD95 ligand interactions, which have been proposed to induce apoptosis in T cells infiltrating immunologically privileged sites, nor CD30 signaling was responsible for the lack of kidney infiltration. When OT-I cells were activated in vitro prior to injection, they could infiltrate the kidney and caused acute renal failure when injected in high numbers. Conclusions. A mechanism distinct from previously described organ-specific protective mechanisms such as sequestration of antigen or CD95-mediated immunoprivilege contributes to the protection of the kidney tubulointerstitium from infiltration by autoreactive CD8+ T cell.
- Publisher
- BLACKWELL SCIENCE INC
- Keywords
- MURINE INTERSTITIAL NEPHRITIS; TUBULAR EPITHELIAL-CELLS; CHRONIC-RENAL-FAILURE; SELF-ANTIGENS; CROSS-PRESENTATION; IN-VIVO; FAS; LYMPHOCYTES; MECHANISMS; DELETION
- Publisher's Version
- https://doi.org/10.1046/j.1523-1755.2001.060002664.x
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- Refer to copyright notice on published article.
Creation Date: 2001-08-01 12:00:00