Date

September 2012

Document Type

Dissertation

Degree Name

Ph.D.

Institution

Oregon Health & Science University

Abstract

Demyelination and axonopathy characterize the central nervous system (CNS) inflammatory disease multiple sclerosis (MS). While the etiology remains unknown, extensive evidence suggests encephalitogenic mononuclear cells mediate disease pathology. A key step in disease onset involves the activation of CD4[superscript +] T-cells that recognize myelin antigens and their extravasation across the blood-brain-barrier (BBB). These cells mediate disease progression by recruiting components of the adaptive immune system that lead to the damage of myelin and axons. These events are recapitulated in a murine model of MS, experimental autoimmune encephalomyelitis (EAE). Therapeutically impairing extravasation of myelin-reactive T-cells in EAE and MS reduces disease severity and recurrence. However, the mechanisms involved in extravasation into the CNS are not completely understood. The extra-cellular matrix (ECM) glycosaminoglycan hyaluronan (HA) and its primary receptor CD44 have been implicated

Identifier

doi:10.6083/M4BV7DNP

Division

Neuroscience Graduate Program

School

School of Medicine

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