Offices of Technology Transfer
Welcome to the web site for the Offices of Technology Transfer. We are the teams who facilitate the protection of Intellectual Property and the commercialization—or transfer—of technologies resulting from the cutting-edge research being conducted by our world-class scientists, faculty, and staff here at the University of Rochester and the University of Rochester Medical Center.
We are here to translate scientific innovation into tangible products or methods that advance knowledge and serve the public good while returning income to the inventor and to the University to support further research.
September 2008: Featured Technology
Disruption of the Signaling Pathway Implicated in the Early Stage Pathogenesis and Recurrence of Multiple Sclerosis (MS)
Early stage in the progression of MS and its animal model, experimental autoimmune encephalomyelitis (EAE), involves the
disruption of the Blood-Brain Barrier (BBB). The BBB is a barrier between the brain tissue and the blood, formed by the
interaction between astrocytes and vascular tissue, and as such regulates the passage of materials (metabolites, cells,
etc.) from blood into the brain. Intact BBB is essential for normal brain function and pathogenic and toxicological
defense. In MS and EAE, the BBB is disrupted and allows for easy translocation of myelin basic protein (MBP) sensitized
T-cells that attack and destroy the brain white matter (BWM). The destruction of BWM, the oligodendrocyte-produced
myelin sheets that insulate neuronal axons, disrupts signal conduction along nerve fibers and results in the symptomatic
neurological problems observed in MS and EAE.
This technology aims to prevent and treat MS by inhibiting the signaling pathway involved in BBB disruption. This is
accomplished by treating the MS patients and EAE animals with an anti-CXCR2 antibody, which prevents the interaction
between the CXCR2 chemokine receptor (found on the surface of granulocytes) and the CXCL1/2 chemokines. The CXCR2-CXCL1/2
chemoattractant signaling pair is responsible for granulocyte homing to the brain vasculature where they act to disrupt the
BBB. Alternatively, the inhibition of this pathway is accomplished by anti-IL17 or anti-IL23 antibodies. By inhibiting
this signaling pathway, BBB breakdown, clinical presentation and disease relapses are prevented. (J. Exp. Med., 205(4):811,2008)
Unlike the currently available therapies, which aim either to pacify the activated immune system or specifically target
T-cells, the described method prevents the recruitment of immune cells responsible for the disruption of the blood-brain
barrier, thereby preventing the subsequent immuno-attack on the white matter.
For More Information, Contact:
Michael Rusnak
Associate Director, Life Sciences
585.784.8850
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