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Fas on renal parenchymal cells does not promote autoimmune nephritis in MRL mice.

Publication ,  Journal Article
Wada, T; Schwarting, A; Kinoshita, K; Naito, T; Griffiths, RC; Coffman, TM; Kelley, VR
Published in: Kidney Int
March 1999

BACKGROUND: Although Fas on pancreatic islets promotes autoimmune diabetes in mice, the role of Fas expression on kidney parenchymal cells during autoimmune disease is unknown. METHODS: To determine whether Fas on renal parenchymal cells promotes autoimmune renal destruction, we compared apoptosis and pathology in Fas-intact and Fas-deficient kidneys in an autoimmune milieu. For this purpose, we transplanted single, normal kidneys from MRL-++ (Fas-intact) mice (3 months of age) into age-matched, congenic MRL-Faslpr (Fas-deficient) recipients after removal of nephritic kidneys. These Fas-intact kidneys were compared with Fas-deficient nephritic kidneys. RESULTS: There is a progressive increase of FasL on kidney-infiltrating cells and Fas and FasL on renal parenchymal cells in MRL-++ kidneys during engraftment (0, 2, 4-6, and 8 weeks). By comparison, we detected an increase in FasL in MRL-Faslpr kidneys (3 to 5 months of age), whereas Fas was not detectable. The engagement of T cells bearing FasL with Fas expressing tubular epithelial cells (TECs) induced TEC apoptosis in vitro. However, apoptosis and pathology were similar in kidneys (MRL-++, 8 weeks postengraftment vs. MRL-Faslpr, 5 months) with equivalent amounts of FasL-infiltrating cells or FasL TECs, regardless of Fas on renal parenchymal cells. CONCLUSION: The expression of Fas on renal parenchymal cells does not increase apoptosis or promote renal disease in MRL-++ mice. We speculate that the autoimmune milieu evokes mechanisms that mask, counter, or pre-empt Fas-FasL-initiated apoptosis in MRL kidneys.

Duke Scholars

Published In

Kidney Int

DOI

ISSN

0085-2538

Publication Date

March 1999

Volume

55

Issue

3

Start / End Page

841 / 851

Location

United States

Related Subject Headings

  • fas Receptor
  • Urology & Nephrology
  • Reverse Transcriptase Polymerase Chain Reaction
  • Nephritis
  • Mice, Inbred MRL lpr
  • Mice, Congenic
  • Mice
  • Membrane Glycoproteins
  • Kidney Transplantation
  • Immunohistochemistry
 

Citation

APA
Chicago
ICMJE
MLA
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Wada, T., Schwarting, A., Kinoshita, K., Naito, T., Griffiths, R. C., Coffman, T. M., & Kelley, V. R. (1999). Fas on renal parenchymal cells does not promote autoimmune nephritis in MRL mice. Kidney Int, 55(3), 841–851. https://doi.org/10.1046/j.1523-1755.1999.055003841.x
Wada, T., A. Schwarting, K. Kinoshita, T. Naito, R. C. Griffiths, T. M. Coffman, and V. R. Kelley. “Fas on renal parenchymal cells does not promote autoimmune nephritis in MRL mice.Kidney Int 55, no. 3 (March 1999): 841–51. https://doi.org/10.1046/j.1523-1755.1999.055003841.x.
Wada T, Schwarting A, Kinoshita K, Naito T, Griffiths RC, Coffman TM, et al. Fas on renal parenchymal cells does not promote autoimmune nephritis in MRL mice. Kidney Int. 1999 Mar;55(3):841–51.
Wada, T., et al. “Fas on renal parenchymal cells does not promote autoimmune nephritis in MRL mice.Kidney Int, vol. 55, no. 3, Mar. 1999, pp. 841–51. Pubmed, doi:10.1046/j.1523-1755.1999.055003841.x.
Wada T, Schwarting A, Kinoshita K, Naito T, Griffiths RC, Coffman TM, Kelley VR. Fas on renal parenchymal cells does not promote autoimmune nephritis in MRL mice. Kidney Int. 1999 Mar;55(3):841–851.
Journal cover image

Published In

Kidney Int

DOI

ISSN

0085-2538

Publication Date

March 1999

Volume

55

Issue

3

Start / End Page

841 / 851

Location

United States

Related Subject Headings

  • fas Receptor
  • Urology & Nephrology
  • Reverse Transcriptase Polymerase Chain Reaction
  • Nephritis
  • Mice, Inbred MRL lpr
  • Mice, Congenic
  • Mice
  • Membrane Glycoproteins
  • Kidney Transplantation
  • Immunohistochemistry