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Tim-1 promotes cisplatin nephrotoxicity.

Yuji Nozaki1, David J Nikolic-Paterson, Hideo Yagita

  • 1Centre for Inflammatory Diseases, Department of Medicine, Monash University, Clayton, Victoria, Australia.

American Journal of Physiology. Renal Physiology
|August 13, 2011
PubMed
Summary

Inhibiting T cell immunoglobulin mucin 1 (Tim-1) with antibodies reduced cisplatin-induced acute kidney injury. This therapeutic strategy protected kidney function by modulating T cell responses, not direct effects on kidney cells.

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Area of Science:

  • Nephrology
  • Immunology
  • Oncology

Background:

  • Cisplatin chemotherapy frequently causes nephrotoxicity, a complication exacerbated by T cell activity.
  • T cell immunoglobulin mucin 1 (Tim-1), also known as kidney injury molecule-1 (Kim-1) on damaged kidney tubules, modulates T cell responses.

Purpose of the Study:

  • To investigate the role of Tim-1 in cisplatin-induced acute kidney injury.
  • To evaluate the therapeutic potential of inhibiting Tim-1 using an anti-Tim-1 antibody.

Main Methods:

  • Administration of an inhibitory anti-Tim-1 antibody to mice undergoing cisplatin chemotherapy.
  • Assessment of kidney function, histology, immune cell infiltration, and molecular markers of inflammation and apoptosis.
  • Studies in Rag1(-/-) mice to differentiate between T cell-dependent and independent effects.

Main Results:

  • Anti-Tim-1 antibody treatment significantly attenuated cisplatin nephrotoxicity, reducing kidney damage and improving renal function.
  • Reduced leukocyte infiltration, NF-κB activation, apoptosis, and pro-inflammatory cytokine/chemokine expression in the kidneys.
  • Inhibition of Tim-1 decreased systemic T cell activation, apoptosis, and cytokine production.
  • Protective effects were T cell-dependent, as anti-Tim-1 antibodies did not benefit Rag1(-/-) mice.

Conclusions:

  • Tim-1 plays a critical role in promoting cisplatin-induced acute kidney injury through T cell modulation.
  • Inhibiting Tim-1 represents a promising therapeutic strategy to prevent or mitigate chemotherapy-induced kidney damage.