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My Research
Multiple sclerosis is a highly heterogeneous disease with significant variability in the clinical course to the pathological patterns observed in brain lesions. Clinically, the heterogeneity in MS is illuminated by the variability in response to interferon-β (IFN-β) therapy. Even though there are clear responders and non-responders to IFN-β, there are limited tools to predict and monitor responsiveness. My laboratory works to identify the biological pathways that impact response to IFN-β therapy.
Our research has shown that specific immune pathways driving neuro-inflammation have clinically significant consequences. We demonstrated that disease phenotypes with elevated TH17/neutrophil signatures, unlike Th1-driven disease, do not respond well to conventional MS therapies. Clinically, these include highly inflamed relapsing remitting MS, neuromyelitis optica (NMO), and progressive MS. Currently, there is a lack of effective treatment options for progressive MS and NMO. Therefore, further characterization of these diseases will provide insights into novel treatment strategies for these underserved patients.
Neuro-autoimmune patients who do not respond to conventional therapies have a strong auto-reactive TH17 response that initiates the recruitment of neutrophils and other inflammatory myeloid cells into the CNS where they support the proliferation of inflammatory B-cells. In contrast, patients who are effectively managed with conventional therapies have a TH1-predominant disease where B-cells have a regulatory response. My studies have addressed three key issues in the field of MS/neuro-inflammation.
- The biological heterogeneity in the MS population impacts the prognosis of this disease. Our studies have identified a series of serum-based biomarkers that could have prognostic utility in MS.
- The balance of inflammatory and regulatory B-cells are key in modulating disease activity in MS. Considering that therapies specifically targeting B-cells are emerging for MS, our studies on B-cell populations are highly relevant and could impact how patients are monitored while on B-cell depleting therapies.
- Our studies have described an underappreciated role of BAFF in TH1- and TH17-induced inflammation, which has provided a plausible explanation for the failure of Atacicept in MS.
Research Keywords
- Multiple sclerosis
- Autoimmune disease
Contact
Robert Axtell, Ph.D.
Arthritis & Immunology Research Program, MS 24
Oklahoma Medical Research Foundation
825 N.E. 13th Street
Oklahoma City, OK 73104
Phone: 405-271-2354
Fax: 405-271-4110
