More about
Dr. James:

Dr. James' profile

Dr. James 101
(for non-scientists)

Dr. James' CV in brief

Publications

COBRE on Science in a Culture of Mentoring

Clinical Immunology Research Program

Dr. James In The News

OMRF chosen as one of nine Autoimmunity Centers of Excellence nationwide

OMRF adds new patient-oriented Clinical Immunology Research Program

Judith A. James, M.D., Ph.D. Member, Clinical Immunology Research Program Lou C. Kerr Chair in Biomedical Research Professor, Department of Medicine, University of Oklahoma Health Sciences   Center Adjunct Professor, Department of Pathology, University of Oklahoma Health   Sciences Center

Over the past several years, our laboratory has been very interested in how a person's immune system can "go awry" and produce autoimmune diseases, such as systemic lupus erythematosus, scleroderma, multiple sclerosis, rheumatoid arthritis, and others.  Systemic lupus erythematosus (SLE) is often considered the "prototype" of autoimmune disease and is characterized by the presence of high concentrations of autoantibodies.  Unfortunately, the role of these autoantibodies in the onset and progression of lupus is unknown.

Our laboratory is approaching understanding these autoantibodies from several different directions.  First, we describe the initial targets of these aberrant self-antibodies by testing serially collected serum samples from patients.  These results have led to the description of a new "peptide-induced" animal model of SLE.  Currently we are using this induced animal model to decipher which genes are involved in this animal model, as well as to understand which cells of the immune system play a role in this disease process.  One of these genes in involved in how subsets of cells in the immune system talk to one another.  Ongoing research is focused on understanding how these interactions do not lead to the appropriate dampening of immune responses and these abnormal responses could be modified for lupus treatment.  From these studies we have also found a very powerful association between being previously exposed to Epstein-Barr virus (EBV) and developing SLE.  In addition, we have found that lupus patients mount a distinctly different immune response to EBV proteins compared to normal controls.  We are currently working on various mechanisms of how this virus may play a role in SLE.  Our research group is also focusing efforts to understand how autoantibodies are involved in major organ damage and the genetic predisposition to these responses.  Finally, based upon our autoimmune disease experience, we have begun to apply parallel approaches to understand other autoimmune diseases (such as scleroderma, multiple sclerosis and rheumatoid arthritis), as well as normal immune responses to vaccinations, such as anthrax and influenza.