Dr Robert Axtell received his bachelor’s and master’s degrees in microbiology at Idaho State University in Pocatello, Idaho. He then earned his PhD at the University of Alabama at Birmingham and completed his post-doctoral training with Dr Lawrence Steinman at Stanford University in California.
He recently joined the Oklahoma Medical Research Foundation in Oklahoma City as an Assistant Member in the division of Arthritis and Clinical Immunology. Dr Axtell’s research utilizes animal models and patient specimens to gain insight into the molecular and cellular mechanisms that drive the heterogeneous nature of multiple sclerosis.
Role of BAFF and APRIL in neuro-inflammatory disorders
In autoimmunity, the function of B cells is highly nuanced. This has been illuminated by clinical trials of therapies that target B cells. B cells, BAFF, and APRIL can be proinflammatory or anti-inflammatory depending on the context of the autoimmune disease.
We have developed two versions of experimental autoimmune encephalomyelitis (EAE) that differ in response to IFN-β. EAE induced with myelin-specific T helper type 1 cells (TH1-EAE) seems to be effectively treated with IFN-β. Conversely, TH17-EAE appears to be exacerbated when treated with IFN-β. We have preliminary data showing elevated expression of BAFF and APRIL and increased B-cell numbers in the central nervous system of TH17-EAE compared with TH1-EAE.
These data suggest that BAFF, APRIL, and B cells have opposing roles in TH1- and TH17-induced EAE: they appear to be proinflammatory in TH17-EAE but anti-inflammatory in TH1-EAE. Our research will investigate the effects of pharmacologically blocking BAFF and APRIL in our two EAE models.
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