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Expression of heat shock protein-65 by oligodendrocytes in vivo and in vitro

Implications for multiple sclerosis

Departments of Pathology (Neuropathology), Neurology, and Neuroscience, and the Rose F. Kennedy Center for Research in Mental Retardation and Human Development, Albert Einstein College of Medicine, Bronx, NY.

We studied immunoreactivity for heat shock proteins (HSPs) in multiple sclerosis (MS) brain tissue and detected HSP-65 in chronic MS plaques at the edge of thinly myelinated (or remyelinated) areas. Serial-section immunocytochemistry and double staining revealed that HSP-65⁺ cells represented reactive, immature oligodendrocytes with strong reactivity for myelin basic protein and weak reactivity for galactocerebroside. Mature oligodendrocytes outside MS plaques did not stain for HSP-65. Control brain sections showed no HSP-65 reactivity. Oligodendrocytes expressed HSP-65 in mixed glial cell cultures. In this system in vitro, oligodendrocytes, but not astrocytes, showed constitutive expression of HSP-65. There was immunoreactivity for HSP-72 in astrocytes in MS and non-MS brains to a similar extent but no association between HSP-72 reactivity and MS plaques. Interestingly, HSP-65⁺ oligodendrocytes colocalized with T lymphocytes expressing the T-cell receptor (TcR). Since HSP-65 has been implicated as a major antigen recognized by TcR lymphocytes, our findings might represent a new immunologic interaction within MS plaques that leads to the destruction of immature oligodendrocytes involved in remyelination.

Address correspondence and reprint requests to Dr. Cedric S. Raine, Department of Pathology (Neuropathology), K435, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461.

Supported in part by an Advanced Fellowship from the National Multiple Sclerosis Society (FG 795-A-1) to K.S.; by NMSS research grants RG 1001-G-7 and 1089-F-9; and by HHS grants NS 08952 and NS 11920.

Received July 22, 1991. Accepted for publication in final form September 20, 1991.

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