Invited Faculty
  • John B. Harley
    Univ. of Cincinnati (Retired)
  • John Harley has focused his research on the genetic and environmental etiologies of autoimmune diseases, especially systemic lupus erythematosus (SLE). After an MD and PhD in Biochemistry from the University of Pennsylvania, postdoctoral fellowship at the Imperial Cancer Research Fund in Tumour Virology, Internal Medical Residency at Yale University, and Clinical Investigator fellowships at the National Institutes of Health, he worked at the University of Oklahoma and the Oklahoma Medical Research Foundation, then at Cincinnati Children’s Hospital Medical Center and the University of Cincinnati. He is now with the US Department of Veterans Affairs Medical Center in Cincinnati. Work on the immunochemistry of SLE autoimmunity identified the earliest autoantigenic structures and nominated the heteroimmune response to Epstein-Barr virus nuclear antigen 1 (EBNA1) as the origin for selected autoimmune responses in SLE. The two decades of subsequent work on the genetic origins of SLE contributed to the discovery of the over 200 risk loci convincingly associated with SLE now known. The accumulating results are building a convincing circumstantial case for Epstein-Barr being important in the initiation of lupus autoimmunity.
    Research & Clinical Focus

    The etiology and pathogenic mechanisms of systemic lupus erythematosus

  • Date Time Room Session Title Lecture Title
    Oct 22 11:00-11:30 Room A [International Symposium] “State-of-the-art” in Systemic Lupus Erythematosus Molecular mimicry & genetic mechanisms implicate Epstein-Barr virus as the major environmental factor causing systemic lupus erythematosus