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The Journal of Neuroscience, May 1, 1999, 19(9):3440-3447
Fc RII/CD23 Is Expressed in Parkinson's Disease and
Induces, In Vitro, Production of Nitric Oxide and Tumor
Necrosis Factor- in Glial Cells
Stéphane
Hunot1,
Nathalie
Dugas2,
Baptiste
Faucheux1,
Andreas
Hartmann1,
Marc
Tardieu2,
Patrice
Debré3,
Yves
Agid1,
Bernard
Dugas3, 4, and
Etienne C.
Hirsch1
1 Institut National de la Santé et de la
Recherche Médicale, Unité 289, Mécanismes et
Conséquences de la Mort Neuronale, Hôpital de la
Salpêtrière, F-75013 Paris, France,
2 Laboratoire "Virus, Neurone et Immunité,"
Unité de Formation et de Recherche Kremlin Bicêtre, F-94276
Le Kremlin-Bicêtre Cedex, France, 3 Centre National
de la Recherche Scientifique, Unité de Recherche Associée
625, Laboratoire d'Immunologie Cellulaire et Tissulaire,
Hôpital de la Salpêtrière, F-75013 Paris, France,
and 4 Oxykine Therapeutics, F-75116 Paris, France
Oxidative stress is thought to be involved in the mechanism of
nerve cell death in Parkinson's disease (PD). Among several toxic
oxidative species, nitric oxide (NO) has been proposed as a key element
on the basis of the increased density of glial cells expressing
inducible nitric oxide synthase (iNOS) in the substantia nigra (SN) of
patients with PD. However, the mechanism of iNOS induction in the CNS
is poorly understood, especially under pathological conditions. Because
cytokines and Fc RII/CD23 antigen have been implicated in the
induction of iNOS in the immune system, we investigated their role in
glial cells in vitro and in the SN of patients with PD
and matched control subjects. We show that, in vitro,
interferon- (IFN-) together with interleukin-1 (Il-1) and
tumor necrosis factor- (TNF-) can induce the expression of CD23
in glial cells. Ligation of CD23 with specific antibodies resulted in
the induction of iNOS and the subsequent release of NO. The activation
of CD23 also led to an upregulation of TNF- production, which was
dependent on NO release. In the SN of PD patients, a significant
increase in the density of glial cells expressing TNF-, Il-1, and
IFN- was observed. Furthermore, although CD23 was not detectable in the SN of control subjects, it was found in both astroglial and microglial cells in parkinsonian patients. Altogether, these data demonstrate the existence of a cytokine/CD23-dependent activation pathway of iNOS and of proinflammatory mediators in glial cells and
their involvement in the pathophysiology of PD.
Key words:
inflammation; iNOS; astrocytes; microglial cells; neurodegenerative disease; postmortem
Copyright © 1999 Society for Neuroscience 0270-6474/99/1993440-08$05.00/0
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