William Robinson

Clinical Focus

• Immunology and Rheumatology
• Rheumatology

Professional Education

Postdoctoral Advisees

Lisa Blum,  Lisa Blum,  Daisuke Harada,  Chia-Hsin Ju,  Chia-Hsin Ju,  Yong Gil Kim,  Dong Sohn

Graduate & Fellowship Program Affiliations

• Immunology
• Medicine

Internet Links

• Robinson Lab

Industry Relationships

Stanford is committed to ethical and transparent interactions with our industrial and other commercial partners. It is our policy to disclose payments (exclusive of travel support) from, and/or equity in, companies or other commercial entities to Stanford faculty of $5,000 or more in total value, as well as any equity in a privately held company, when the faculty member also has institutional responsibilities related to his or her interactions with the company. View Full Information

Current Research Interests

Research Overview

Our laboratory is pursuing two major lines of research.

1. The first is the study of autoimmunity. Autoimmune diseases affect 3-5% of the world population, yet the pathogenesis of most autoimmune diseases is unclear. Moreover, current therapies globally modulate immune function, resulting in potentially fatal side effects, and are not curative, serving only to slow disease progression.

• A major objective of our research is to understand the mechanisms underpinning the initiation, natural remission, and progression of autoimmune diseases—particularly of rheumatoid arthritis (RA) and multiple sclerosis (MS)—and to develop targeted therapeutics that cure these diseases without incurring serious adverse side effects.

• Another important goal is to develop biomarker assays that can guide therapeutic decision-making in clinical practice. Effective treatment of RA and MS has been impeded by the heterogeneity of the diseases—by identifying molecular ‘signatures’ of disease subtypes, we hope to ultimately develop clinical tests that enable therapy to be tailored to the individual patient.


2. The second line of research is the study of osteoarthritis (OA), the most common form of arthritis. Unlike RA, OA is not an autoimmune disorder and is generally believed to result from ‘wear and tear’. However, inflammation is emerging as an important component of OA, prompting a reassessment of our understanding of OA pathology. This recent discovery has raised a slew of intriguing questions about the role of inflammation in OA and suggested new possibilities for therapeutic intervention.

• We are working to elucidate the pathogenesis of and develop therapies for OA, a disorder for which there is currently no treatment other than pain alleviation.

Clinical Trials

• A Pilot Study of Imatinib Mesylate in Steroid Refractory Chronic Graft Versus Host Disease No longer recruiting

Publications

• Blood autoantibody and cytokine profiles predict response to anti-tumor necrosis factor therapy in rheumatoid arthritis. Hueber W, Tomooka BH, Batliwalla F, Li W, Monach PA, Tibshirani RJ, Van Vollenhoven RF, Lampa J, Saito K, Tanaka Y, Genovese MC, Klareskog L, Gregersen PK, Robinson WH. Arthritis Res Ther. 2009; 11 (3): R76
• Molecular framework for response to imatinib mesylate in systemic sclerosis. Chung L, Fiorentino DF, Benbarak MJ, Adler AS, Mariano MM, Paniagua RT, Milano A, Connolly MK, Ratiner BD, Wiskocil RL, Whitfield ML, Chang HY, Robinson WH. Arthritis Rheum. 2009; 60 (2): 584-91
• Tyrosine kinases as targets for the treatment of rheumatoid arthritis. D'Aura Swanson C, Paniagua RT, Lindstrom TM, Robinson WH. Nat Rev Rheumatol. 2009; 5 (6): 317-24
• Proteomic analysis of active multiple sclerosis lesions reveals therapeutic targets. Han MH, Hwang SI, Roy DB, Lundgren DH, Price JV, Ousman SS, Fernald GH, Gerlitz B, Robinson WH, Baranzini SE, Grinnell BW, Raine CS, Sobel RA, Han DK, Steinman L. Nature. 2008; 451 (7182): 1076-81
• Lipid microarrays identify key mediators of autoimmune brain inflammation. Kanter JL, Narayana S, Ho PP, Catz I, Warren KG, Sobel RA, Steinman L, Robinson WH. Nat Med. 2006; 12 (1): 138-43