Hauser is a principal investigator of a multinational effort to identify genetic effects on MS. He is 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
major histocompatibility complex (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 been mapped. Hauser has contributed to the development of B-cell–targeted therapies for multiple sclerosis (MS). He led a clinical trial investigating
rituximab, a monoclonal antibody targeting CD20+ B cells, which demonstrated efficacy in relapsing-remitting MS. A subsequent trial in primary progressive MS suggested that rituximab may be beneficial in a subset of patients with evidence of active inflammation. A related trial using
ocrelizumab, a humanized anti-CD20 antibody, reported similar findings in relapsing-remitting MS. Hauser has also participated in efforts to apply precision medicine to MS. As part of this work, he co-developed the MS BioScreen, a data integration tool designed to support individualized monitoring and decision-making in MS care. ==Service==