Inhibitor of apoptosis protein (IAP) profiling in experimental autoimmune encephalomyelitis (EAE) implicates increased XIAP in T lymphocytes

Craig S. Moore, Andrea L.O. Hebb, George S. Robertson

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)

Abstract

In multiple sclerosis (MS) and its widely accepted animal model, experimental autoimmune encephalomyelitis (EAE), the failure of autoreactive immune cells to undergo apoptosis is thought to contribute to CNS tissue damage and disease progression. Promoting apoptosis of myelin-reactive immune cells in diseases such as MS, may delay disease progression and decrease the frequency and severity of relapses. X-linked inhibitor of apoptosis (XIAP) is a potent anti-apoptotic protein that inhibits intrinsic, extrinsic, and c-Jun amino-terminal kinase mediated apoptosis and was the only member of the inhibitor of apoptosis (IAP) family upregulated in whole blood from EAE mice. Similar increases in XIAP were also observed in both peripheral and encephalitogenic T lymphocytes. Increased XIAP expression in T cells within areas of demyelination in the CNS suggests that XIAP may be enhancing cell survival and thereby contributing to disease pathology.

Original languageEnglish
Pages (from-to)94-105
Number of pages12
JournalJournal of Neuroimmunology
Volume193
Issue number1-2
DOIs
Publication statusPublished - Jan 2008

Bibliographical note

Funding Information:
The authors would like to thank the Merck Frosst Centre for Therapeutic Research and D.W. Nicholson for the generation and donation of the anti-caspase cleaved spectrin antibody. This study was supported by Genome Canada and Aegera Therapeutics Inc. CSM holds a research studentship from the Multiple Sclerosis Society of Canada. ALOH holds a post-doctoral fellowship from the Multiple Sclerosis Society of Canada.

ASJC Scopus Subject Areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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