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Tracking of myelin‐reactive T cells in experimental autoimmune encephalomyelitis (EAE) animals using small particles of iron oxide and MRI
Author(s) -
Baeten Kurt,
Adriaensens Peter,
Hendriks Jerome,
Theunissen Evi,
Gelan Jan,
Hellings Niels,
Stinissen Piet
Publication year - 2010
Publication title -
nmr in biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.278
H-Index - 114
eISSN - 1099-1492
pISSN - 0952-3480
DOI - 10.1002/nbm.1501
Subject(s) - experimental autoimmune encephalomyelitis , myelin , multiple sclerosis , chemistry , encephalomyelitis , central nervous system , spinal cord , demyelinating disease , myelin oligodendrocyte glycoprotein , pathology , immunology , biology , medicine , endocrinology , neuroscience
Myelin‐reactive T cells are responsible for initiating the cascade of autoreactive immune responses leading to the development of multiple sclerosis. For better insights into the disease mechanism, it is of major importance to have knowledge on the sites at which these cells are active during disease progression. Herein, we investigated the feasibility of tracking myelin‐reactive T cells, upon labelled with SPIO particles, in the central nervous system (CNS) of experimental autoimmune encephalomyelitis (EAE) animals by MRI. First, we determined the optimal labelling condition leading to a high particle uptake and minimal SPIO–Poly‐l‐lysine (PLL) aggregate formation using Prussian blue staining and inductively coupled plasma spectroscopy measurements. Results from labelling of myelin reactive T cells with low concentrations of SPIO particles (i.e. 25 µg/ml) combined with different concentrations of PLL (0–1.5 µg/ml) showed that increasing amounts of PLL led to augmented levels of free remnant SPIO‐PLL aggregates. In contrast, a low PLL concentration (i.e. 0.5 µg/ml) combined with high concentrations of SPIO (i.e. 400 µg Fe/ml) led to a high labelling efficiency with minimal amounts of aggregates. Second, the labelled myelin‐reactive T cells were transferred to control rats to induce EAE. At the occurrence of hindlimb paralysis, the SPIO labelled myelin‐reactive T cells were detected in the sacral part of the spinal cord and shown to be highly confined to this region. However, upon transfer in already primed rats, T cells were more widely distributed in the CNS and shown present in the spinal cord as well as in the brain. Our study demonstrates the feasibility of tracking SPIO labelled myelin‐reactive T cells in the spinal cord as well as the brain of EAE rats upon systemic administration. Furthermore, we provide data on the optimal labelling conditions for T cells leading to a high particle uptake and minimal aggregate formation. Copyright © 2010 John Wiley & Sons, Ltd.