Post-Doc Spotlight

Post Doc Spotlight, Fall 2012: Andrew Steelman

I attended Gardner-Webb University in North Carolina, where I received Bachelor of Science degree in Biology in 2002. Subsequently, I completed the professional program in biotechnology earning a Master's degree in biotechnology and a certificate in business from Texas A&M University in 2003. Finally, I obtained a Ph.D. degree in biomedical science from Texas A&M University in 2008, in part for research pertaining to the effects of stress on immune responses to Theiler's murine encephalomyelitis virus, an animal model of multiple sclerosis. I am currently a post-doctoral fellow working in Dr. Jianrong Li's laboratory at Texas A&M University on glial responses that occur during demyelinating disease, particularly multiple sclerosis and its animal models.

Multiple sclerosis (MS) is a complex chronic disease of the central nervous system, characterized by demyelination and neurodegeneration. Both genome wide association studies and clinical treatment strategies implicate peripheral immune cells as the underlying cause of early disease progression. Indeed, it is generally believed that MS is a T-cell mediated autoimmune disease that is triggered by environmental factors such as infection. As such, a great deal of research has focused on limiting the aberrant inflammatory response that occurs within the CNS in attempts to quench the ongoing pathology. Approaches aimed at limiting CNS inflammation include; promoting Treg cell polarization and effector function, inhibiting inflammatory cell trafficking into the CNS and inducing tolerance in the periphery, all of which prove efficacious when tested in animal models such as experimental autoimmune encephalomyelitis. Yet, little is known about the role of glia during CNS inflammation and in particular how glia contribute to the pathology and/or resolution of MS. This is especially true when considering molecular cross-talk between the cells that comprise the adaptive immune system (i.e. B-cells, T-cells) and resident glia (i.e. oligodendrocytes, astrocytes and to a lesser extent microglia).

As such, I am interested in the outcomes of the glial-immune cell cross talk that occurs following both acute CNS inflammation (such as viral encephalitis) as well as chronic CNS inflammation (multiple sclerosis) and how these intracellular communication pathways contribute to pathology as well as tissue repair. Understanding the basic physiological responses of resident glia following an inflammatory insult will likely lead to a more comprehensive view on how the CNS maintains an 'immune privilege' status and is able to partially restore homeostasis after an insult. The long-term goal would be to exploit such pathways to achieve a therapeutically beneficial outcome for those suffering from inflammatory mediated degenerative CNS diseases such as multiple sclerosis.

It is an honor to have received pre-doctoral funding from the NIH as well as post-doctoral grant seed funding from the College of Veterinary Medicine and a fellowship from the National Multiple Sclerosis Society. It is also an honor to have been selected by the post-doctoral association at the University of Georgia to present my current findings as a part of the S.I.T.E. program. One of my biggest accomplishments is completing the MS 150 in part for a friend of mine that has MS.