Mark J. Soloski, PhD
Professor of Medicine
Co-Director for Basic Research, Lyme Disease Research Center
Johns Hopkins School of Medicine
Host Immune Response in Lyme Borreliosis
Mark J. Soloski, Ph.D., is currently a Professor of Medicine in the Division of Rheumatology at the Johns Hopkins University School of Medicine and he holds joint appointments in the School of Medicine’s Departments of Pathology and Molecular Biology and Genetics as well as the Department of Molecular Microbiology and Immunology in the School of Public Health. He is the Co-Director for Basic Research for the Johns Hopkins Lyme Disease Research Center. Dr. Soloski received his Ph. D. in Microbiology from Rutgers, the State University of New Jersey and then completed post-doctoral training in Immunology at the University of Texas Health Science Center at Dallas, Southwestern Medical School prior to joining the faculty at the Johns Hopkins School of Medicine in 1983. The overarching theme of his research is understanding how infection can lead to long-term persistent symptoms. At this time, working with John Aucott, M.D. the Director of the Lyme Center at Hopkins, he is focused on understanding how the immune system contributes to the symptoms and severity of Human Lyme disease. He is very active and excited about the teaching of students, at all levels, about how the immune system evolved, how it protects us from infection and how it can contribute to disease.
Conference Lecture Summary
Lyme disease is an inflammatory illness initiated by infection with Borrelia burgdorferi following a bite from an infected tick. Over the last four decades, the number of Lyme disease cases has risen sharply and it is now the most common vector-borne disease in the United States with over 300,000 cases each year. Symptoms of early Lyme disease can range from erythema migrans (EM) alone to systemic toxicity with signs of disseminated infection. Further, a number of patients with undetected and untreated early Lyme disease will develop late-onset musculoskeletal or neurological symptoms. While the acute infection and late-onset disease can be controlled by antibiotic therapy, in a subset of patients, arthritis with inflammation can be antibiotic-refractory. In addition, 10-20% of patients treated for early Lyme disease develop Post-Treatment Lyme Disease Syndrome (PTLDS), a condition with an unknown pathophysiological etiology that may have an immune component. The rising incidence of Lyme disease as well as the complexity of disease outcomes demands a deeper understanding of the immune-mediated process triggered by infection with B. burgdorferi.
In this presentation the current knowledge of the host immune response to B. burgdorferi in human Lyme disease will be reviewed with particular attention to how variation in host immunity may play a role in driving persistent symptoms versus return to health. Data from the study of the Johns Hopkins Slice cohort will also be presented that will address our hypothesis that the nature of the immune response plays a key role in the range of pathophysiological outcomes in human Lyme disease.