Dr. Johnson completed her doctoral degree from the Johns Hopkins School of Medicine in the Pathobiology Graduate Training Program with a focus on infectious diseases of the CNS. She completed a postdoctoral fellowship at the NIH where she developed an interest in autoimmune diseases of the CNS. This prompted her to pursue additional training in Rheumatology and immunology at the Johns Hopkins School of Medicine where she developed a broad portfolio of projects centered on investigating autoimmune disease mechanisms. In 2016 Dr. Johnson joined the Department of Neurology at the Johns Hopkins University School of Medicine as an Assistant Professor. Dr. Johnson’s research is focused on understanding the burden and mechanism of autoimmune CNS diseases and the potential links of autoimmune disease processes to infectious diseases. Studies investigating the neurotoxic properties of a recently identified autoantibody in Nodding Syndrome, a unique form of epilepsy, are currently underway. These studies are focused on understanding the molecular mechanisms by which these antibodies causes neuronal dysfunction and death, characterizing the expression of the antigen in the human brain and modeling the formation and consequences of these autoantibodies in a murine model. Her lab currently collaborates within the Department of Neurology for autoantigen discovery in suspected autoimmune CNS diseases using both biochemical and bioinformatics approaches. Once identified, additional studies to understand the mechanisms of pathogenic immune cells and antibodies are undertaken using cellular and animal models. Dr. Johnson has additional collaborations with investigators in the Division of Rheumatology and Department of Pathology focused on understanding the contribution of autoimmunity and inflammation to CNS disease.
In an independent area of investigation, the Johnson Lab also studies the mechanism by which the HIV-1 protein Tat induces neuroinflammation. Dr. Johnson has previously demonstrated that Tat is expressed by virally infected cells despite anti-retroviral therapy and that Tat can be detected in the CSF of patients with HIV-1. Additionally, the presence of Tat is capable of inducing T-cells to become active and secrete IL-17, a pro-inflammatory cytokine. Further studies to understand the mechanism by which Tat activates T-cells and to characterize their role in the development of HIV-associated neurocognitive disorders (HAND) are currently underway.