Activated effector and memory T cells contribute to circulating sCD30: Potential marker for islet allograft rejection

D. Saini, S. Ramachandran, A. Nataraju, N. Benshoff, W. Liu, N. Desai, W. Chapman, T. Mohanakumar

Research output: Contribution to journalArticle

26 Scopus citations

Abstract

T-cell activation up-regulates CD30 resulting in an increase in serum soluble CD30 (sCD30). CD4+ T cells, a major source for sCD30, play a significant role in the pathogenesis of rejection. In this study, sCD30 was measured pre- and posttransplant in mouse islet allograft models and human islet allograft recipients. sCD30 was measured by ELISA in diabetic C57BL/6, CD4Knockout (KO) and CD8KO islet allograft recipients. sCD30 increased significantly prior to rejection (1.8 ± 1 days) in 80% of allograft recipients. Sensitization with donor splenocytes, or a second graft, further increased sCD30 (282.5 ± 53.5 for the rejecting first graft vs. 374.6 ± 129 for the rejecting second graft) prior to rejection suggesting memory CD4+ T cells contribute to sCD30. CD4KO failed to reject islet allograft and did not demonstrate sCD30 increase. CD8KO showed elevated (227 ± 107) sCD30 (1 day) prior to rejection. High pretransplant sCD30 (>20 U/ml) correlated with poor outcome in human islet allograft recipients. Further, increase in sCD30 posttransplant preceded (3-4 months) loss of islet function. We conclude that sCD30 is released from activated CD4 T cells prior to islet allograft rejection and monitoring sCD30 can be a valuable adjunct in the follow-up of islet transplant recipients.

Original languageEnglish
Pages (from-to)1798-1808
Number of pages11
JournalAmerican Journal of Transplantation
Volume8
Issue number9
DOIs
StatePublished - Sep 1 2008

Keywords

  • CD30 antigen
  • Graft survival
  • Islets
  • Sensitization
  • T-cell activation

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