Abstract
Alpha-fetoprotein (AFP) is an immunomodulatory glycoprotein associated with the normal
growth of the mammalian fetus. Ws have shown that treatment with recombinant human
AFP (rhAFP) reduced lymphocyte reactivity and the extent of neuroinflammation in mice
with experimental autoimmune encephalomyelitis (EAE). In the present study we found
involvement of AFP in immune cell apoptosis, attesting to its possible mechanism of
action. AFP increased the expression of the Bax, Bid, Bad and ApaF genes in peripheral
lymphocytes, together with an enhanced expression of Caspase-3, Fas, FasL and TRAIL
among infiltrating immune cells. The induction of apoptosis markers was accompanied
with an increased expression of Foxp3 in lymph node cells, as well as accumulation
of CD4+Foxp3+ regulatory T cells in the CNS. Overall, these immunological alterations gave
rise to a milder disease and accelerated remission rate. Our results suggest a new
role for AFP in controlling the autoimmune inflammation associated with EAE.
Keywords
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Article info
Publication history
Published online: January 27, 2009
Accepted:
December 9,
2008
Received in revised form:
November 16,
2008
Received:
July 2,
2008
Identification
Copyright
© 2008 Elsevier B.V. Published by Elsevier Inc. All rights reserved.