Cytotoxic molecule mRNA expression in chronically rejected human kidney allografts

Transplant Proc. 2005 Jul-Aug;37(6):2476-8. doi: 10.1016/j.transproceed.2005.06.077.

Abstract

The pathogenesis of immunological and nonimmunological components that cause chronic kidney allograft nephropathy (CAN), is not yet completely understood. To explore the possible contribution of alloreactive cytotoxic T cells, we analyzed the transcription of cytotoxic molecules such as granzyme B and perforin using semiquantitative RT-PCR on surgically removed grafts obtained from two groups: group 1 (n = 10) were cases of CAN; group 2 (n = 3) had no CAN. Among group 1 kidneys, granzyme-B was expressed in 7 of 10, whereas perforin was detectable in 9 of 10 cases; their detection was not related to the presence of superimposed signs of acute graft lesions. Cytotoxic molecules were never found in group 2 kidneys. These results show that explanted chronically rejected grafts display cytotoxic molecule transcripts in addition to Th2 type cytokines, such as IL-10, IL-3, and IL-6, suggesting that both cellular and humoral alloreactive mechanisms may play important roles in CAN pathogenesis.

MeSH terms

  • Antigens, CD / genetics
  • Base Sequence
  • Chronic Disease
  • Cytokines / genetics*
  • DNA Primers
  • Graft Rejection / genetics
  • Graft Rejection / immunology*
  • Granzymes
  • Humans
  • Interleukins / genetics*
  • Kidney Transplantation / immunology*
  • Kidney Transplantation / pathology
  • RNA, Messenger / genetics*
  • Serine Endopeptidases / genetics
  • T-Lymphocytes, Cytotoxic / immunology
  • Transplantation, Homologous / immunology

Substances

  • Antigens, CD
  • Cytokines
  • DNA Primers
  • Interleukins
  • RNA, Messenger
  • GZMB protein, human
  • Granzymes
  • Serine Endopeptidases