Abdolmohamad Rostami, MD, PhD
Nicholas Maiale Distinguished Professor and Chair
Chairman, Department of Neurology
Director, Neuroimmunology Laboratory
Contact
901 Walnut Street
Suite 400
Philadelphia, PA 19107
215-955-8100
215-955-1390 fax
Abdolmohamad Rostami, MD, PhD
Nicholas Maiale Distinguished Professor and Chair
Chairman, Department of Neurology
Director, Neuroimmunology Laboratory
Education
Medical School
MD, Shiraz University, Iran
PhD, University of Pennsylvania
Residency
Hospital of University of Pennsylvania (HUP)
Fellowship
Hospital of University of Pennsylvania (HUP)
Publications
- Retraction Notice to: Neurotrophin 3 Transduction Augments Remyelinating and Immunomodulatory Capacity of Neural Stem Cells (Molecular Therapy (2014) 22(2) (440–450), (S1525001616311650), (10.1038/mt.2013.241))
- Retraction Notice to: Neural Stem Cells Engineered to Express Three Therapeutic Factors Mediate Recovery from Chronic Stage CNS Autoimmunity (Molecular Therapy (2016) 24(8) (1456–1469), (S1525001616335973), (10.1038/mt.2016.104))
- IL-11 induces NLRP3 inflammasome activation in monocytes and inflammatory cell migration to the central nervous system
- Corrigendum: Combination therapy with fingolimod and neural stem cells promotes functional myelination in vivo through a non-immunomodulatory mechanism(Front. Cell. Neurosci., (2019), 13, (14), 10.3389/fncel.2019.00014)
- GATA1 controls numbers of hematopoietic progenitors and their response to autoimmune neuroinflammation
- SIRT1 inactivation switches reactive astrocytes to an antiinflammatory phenotype in CNS autoimmunity
- Transcription Factor RUNX3 Mediates Plasticity of ThGM Cells Toward Th1 Phenotype
- CSF-1 maintains pathogenic but not homeostatic myeloid cells in the central nervous system during autoimmune neuroinflammation
- Engineered extracellular vesicles encapsulated Bryostatin-1 as therapy for neuroinflammation
- Response of Astrocyte Subpopulations Following Spinal Cord Injury
- The effect of 2-amino-3-carboxymuconate-6-semialdehyde decarboxylase gene overexpression in the kynurenine pathway on the expression levels of indoleamine 2,3-dioxygenase 1 and interferon-γ in inflammatory conditions: an in vitro study
- Oral D-mannose treatment suppresses experimental autoimmune encephalomyelitis via induction of regulatory T cells
- The SNX-482 peptide from Hysterocrates gigas spider acts as an immunomodulatory molecule activating macrophages
- IFN-β Acts on Monocytes to Ameliorate CNS Autoimmunity by Inhibiting Proinflammatory Cross-Talk Between Monocytes and Th Cells
- Montelukast alleviates inflammation in experimental autoimmune encephalomyelitis by altering Th17 differentiation in a mouse model
- Role of extracellular vesicles in neurodegenerative diseases
- P7C3 attenuates CNS autoimmunity by inhibiting Th17 cell differentiation
- CRISPR-mediated rapid generation of neural cell-specific knockout mice facilitates research in neurophysiology and pathology
- Chloroquine reduces Th17 cell differentiation by stimulating T-bet expression in T cells
- A serine protease inhibitor suppresses autoimmune neuroinflammation by activating the STING/IFN-β axis in macrophages
Board Certification
American Board of Psychiatry and Neurology
Research & Clinical Interests
Multiple Sclerosis is an autoimmune disease of the central nervous system that affects over 400,000 Americans and over two million worldwide. My research focuses on the pathogenesis of multiple sclerosis using the animal model of this disease, experimental autoimmune encephalomyelitis (EAE). At the present, we are focusing on three main areas:
- The role of IL-12/IL-17/IL-23 axis in the pathogenesis of EAE and multiple sclerosis.
Specifically, studies will examine IL-12/IL-17/IL-23 produced by antigen presenting cells (APC) from the periphery (macrophages and dendritic cells) and from the central nervous system (CNS) microglia in EAE. In addition to a better understanding of the pathogenesis of inflammatory demyelination, the information derived from this study will be helpful if these cytokines are to be considered as targets for therapy in MS. - The effect of the Bowman-Birk protease inhibitor on the course of EAE.
This study has the potential to provide a novel, safe, and effective therapy for multiple sclerosis. - Mechanisms of intravenous tolerance in EAE.
This study will elucidate the mechanisms by which intravenous myelin antigens induce tolerance and suppress clinical disease in EAE. This study will provide a novel method for analyzing the migration and functional status of infiltrating cells in the CNS, in particular, and in target organs of other autoimmune diseases. It has the potential as a possible therapy for autoimmune diseases.