Our research program focuses on projects that seek to understand and optimize daily function, quality of life and health equity for individuals with multiple sclerosis (MS) and related conditions, as well as their families, caregivers and support networks. Our projects include research on cognitive function (e.g., thinking, memory), emotional function (e.g., mood and stress), health behaviors (e.g., self-management of sleep, fatigue, physical activity) and social determinants of health (e.g., healthcare access, socioeconomic status, employment) that affect quality of life in MS.

The Calabresi Lab is located in the department of Neurology at the Johns Hopkins University School of Medicine. Our group investigates why remyelination occasionally fails following central nervous system demyelination in diseases like multiple sclerosis. Our primary focus is on discovering the role of t-cells in promoting or inhibiting myelination by the endogenous glial cells.

The research activities of the Neuroimmunopathology Laboratory focus on studies of immunological and molecular mechanisms involved in the pathogenesis of neurological disorders. Our main areas of research include studies of neurological complications of HIV infection and AIDS, multiple sclerosis, transverse myelitis, autism and epilepsy. We seek to explore and identify immunopathological mechanisms associated with neurological disease that may be the target of potential therapeutic interventions. The laboratory collaborates with other researchers and laboratories at Johns Hopkins and other institutions in projects related with studies of the interaction between the immune and central nervous systems in pathological processes leading to neurological dysfunction.

Our laboratory conducts basic and translational research aimed at better understanding the pathogenesis of multiple sclerosis (MS) and the role of the immune system in CNS disease, particularly the processes that drive progressive disability such as neurodegeneration and remyelination failure. We currently have three parallel research programs: 1. Metabolism as a modulator of MS: We are studying how basic metabolic pathways regulate the immune system and how these pathways might be exploited to protect neurons and myelin-forming oligodendrocytes from injury. 2. Identifying pathways by which nitric oxide (NO) and other free radicals cause neuronal and axonal damage. Our lab is identifying specific signaling pathways initiated by NO and other free radicals that can be targeted by drugs to produce neuroprotection. 3. Modulating the innate immune system in MS: In collaboration with others at Johns Hopkins, we are studying ways to enhance the reparative functions of microglia while preventing maladaptive responses. This work has identified bryostatin-1 as a potential drug that may be re-purposed for this task.

We utilize various multiple sclerosis experimental models to expedite the discovery of innovative therapeutic approaches to stop neurodegeneration and promote remyelination.

Effective immune responses are critical for control of a variety of infectious disease including bacterial, viral and protozoan infections as well as in protection from development of tumors. Central to the development of an effective immune response is the T lymphocyte which, as part of the adaptive immune system, is central in achieving sterilization and long lasting immunity. While the normal immune responses is tightly regulated there are also notable defects leading to pathologic diseases. Inactivity of tumor antigen-specific T cells, either by suppression or passive ignorance allows tumors to grow and eventually actively suppress the immune response. Conversely, hyperactivation of antigen-specific T cells to self antigens is the underlying basis for many autoimmune diseases including: multiple sclerosis; arthritis; and diabetes. Secondary to their central role in a wide variety of physiologic and pathophysiologic responses my lab takes a broad-based approach to studying T cell responses.