Stephen Hauser
| Stephen L. Hauser | |
|---|---|
 |
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| Born |
December 14, 1949 New York, New York, U.S. |
| Nationality | United States |
| Fields | Neurology, neuroimmunology |
| Institutions | University of California, San Francisco |
| Alma mater | Harvard Medical School |
| Known for |
multiple sclerosis research bioethics |
| Notable awards | John Dystel Prize for Multiple Sclerosis Research (2008) Charcot Award (2013) |
Stephen L. Hauser is the Robert A. Fishman Distinguished Professor and Chair of the Department of Neurology at the University of California, San Francisco (UCSF), where his work has focused on immune mechanisms and multiple sclerosis (MS). He was part of the team that identified the role of humoral immunity in the pathogenesis of MS lesions, leading to the development of B-cell based therapies for MS. He has contributed to the establishment of consortia that have identified more than 50 gene variants that contribute to MS risk.
Hauser is a principal investigator of a large multinational effort to identify genetic effects on MS, and part of the team that identified that humoral immune mechanisms are important in the pathogenesis of MS lesions, leading to the development of B-cell based therapies for MS. He has contributed to the establishment of nationwide and international genetics consortia that have identified more than 50 gene variants that contribute to MS risk.
Using comparative genomics between African-American and Caucasian MS populations, Hauser's group was able to identify HLA-DRB1 as the primary MS signal in the MHC, and also fine map other secondary loci in this region.
In 2007, as a senior organizer of the International Multiple Sclerosis Genetics Consortium (IMSGC), he helped identify the first two non-HLA genes involved in MS susceptibility, IL-2R (CD25) and IL-7R (CD127).
In 2010, his laboratory published the complete genome sequences and the epigenome of identical twins discordant for MS. By mid-2011 more than fifty MS associated risk alleles were identified, and by now nearly the entire array of common variants associated with MS susceptibility have now been mapped.
Hauser also has focused on the role of the B cell and immunoglobulin in the pathogenesis of the disease. He developed and characterized an MS disease model that replicated the core feature of vesicular demyelination previously observed in MS, and demonstrated that this pathology resulted from the synergistic effects of autoreactive T-cells and pathogenic autoantibodies. In 1999 he published work identifying specific myelin reactivity of these autoantibodies deposited in areas of myelin damage in MS brains. Hauser has translated this finding into a new potential therapy for MS. He led a large-scale clinical trial with rituximab, a chimeric monoclonal antibody that depletes CD20+ B cells, and demonstrated robust efficacy in relapsing remitting MS. A second trial in primary progressive MS reported in 2009 that rituximab may similarly be effective in patients with primary progressive MS who also have evidence of ongoing inflammatory CNS disease. More recently, a third clinical trial with a fully humanized anti-CD20 monoclonal antibody, ocrelizumab, replicated the results of the rituximab trial in relapsing remitting MS. With the MS Bioscreen project, Hauser has pioneered precision medicine for complex diseases like MS, creating an "actionable digital growth-chart for complex traits"
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