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Alex F. de Vos, Andrew D. Dick, Jan Klooster, Lidy Broersma, Paul G. McMenamin, Aize Kijlstra; Analysis of the Cellular Infiltrate in the Iris during Experimental Autoimmune Encephalomyelitis. Invest. Ophthalmol. Vis. Sci. 2000;41(10):3001-3010.
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purpose. Previous studies have shown that experimental autoimmune
encephalomyelitis (EAE) and anterior uveitis (AU) develop in Lewis rats
immunized with myelin basic protein (MBP). The purpose of this study
was to characterize the dynamics, distribution, and phenotype of
infiltrating cells in the iris during EAE-associated AU.
methods. Lewis rats were immunized with MBP emulsified in complete Freund’s
adjuvant (CFA) or with CFA alone. Cellular infiltration of the iris was
analyzed at various time points by immunohistochemistry of wholemounts,
flow cytometry, and immunoelectron microscopy, by using monoclonal
antibodies specific for monocytes/macrophages (ED1), T lymphocytes
(R73, W3.25, OX8), T-cell activation markers (OX39, OX40), granulocytes
(HIS48), major histocompatibility complex (MHC) class II (OX6), and
results. MBP-immunized rats showed development of characteristic monophasic EAE,
followed, after resolution of paralysis, by mild self-limited AU.
Initially, focal infiltrates of round MHC class II+ and
ED1+ cells were found in the iris. During the course of AU,
the midiris became massively infiltrated with ED1+ monocytes-macrophages, R73+ T cells, granulocytes
(HIS48+), and MHC class II+ cells. The influx
of T cells consisted of CD4+ and CD8+ cells, of
which only a small fraction (<14 and 11%, respectively) expressed
activation markers. The infiltrating cells accumulated in proximity to
myelinated and nonmyelinated nerve bundles and in the vicinity of blood
vessels in the iris. No evidence was found for demyelination or nerve
degradation. Neither EAE nor AU developed in CFA-treated control rats.
conclusions. These data show that EAE-associated AU is characterized by a transient
mixed cellular infiltrate consisting of monocytes-macrophages,
granulocytes, and CD4 and CD8 T cells. The preferential accumulation of
inflammatory cells in the vicinity of nerve fibers suggests that AU in
this model may result from autoreactivity to nerve
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