[Abstract Title]. - Society for Neuroscience

week post injury. The hystological analysis of the nerve confirmed the degeneration process
from the crush area to the distal zone.
The characterisation of cultured BMMCs shows a heterogeneous population of small-rounded,
spindle-shaped and large-flattened morphology; they showed fibroblast-like morphology at
reaching confluence.
After 24-48hs in culture the adherent and non-adherent cells are CD34 + , while adherent cells are
CD45 - , CD11b - , vimentin + , Thy 1.1 + .
Our results demonstrate the existence of a progenitor population in BMMC that spontaneously
migrates to the injured nerve to participate in the degeneration-regeneration process.
Disclosures: V. Usach, None; B. Goitia, None; P.C. Setton-Avruj , None.
Poster
251. Demyelinating Disorders: Animal Models and Human Studies I
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 251.17/W10
Topic: C.08.b. Animal models
Title: Inhibition of midkine alleviates experimental autoimmune encephalomyelitis through the
expansion of regulatory T cell population
Authors: *H. TAKEUCHI, J. WANG, Y. SONOBE, S. JIN, T. MIZUNO, A. SUZUMURA;
Dept Neuroimmunol, Res. Inst. Env Med, Nagoya Univ., Nagoya, Japan
Abstract: CD4+CD25+ regulatory T (Treg) cells are crucial mediators of autoimmune tolerance.
The factors that regulate Treg cells, however, are largely unknown. Here, we show that
deficiency in midkine (MK), a heparin-binding growth factor involved in oncogenesis,
inflammation, and tissue repair, attenuated experimental autoimmune encephalomyelitis (EAE)
due to an expansion of the Treg cell population in peripheral lymph nodes and decreased
numbers of autoreactive T-helper type 1 and T-helper-17 cells. MK decreased the Treg cell
population ex vivo in a dose-dependent manner by suppression of STAT5 phosphorylation that is
essential for Foxp3 expression. Moreover, administration of anti-MK RNA aptamers
significantly expanded the Treg cell population and alleviated EAE symptoms. These
observations indicate that MK serves as a critical suppressor of Treg cell expansion, and
inhibition of MK using RNA aptamers may provide an effective therapeutic strategy against