Philadelphia University + Thomas Jefferson University

Rostami, Abdolmohamad

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Abdolmohamad Rostami, MD, PhD

Abdolmohamad Rostami, MD, PhD

Contact Dr. Rostami

900 Walnut Street
Suite 200
Philadelphia, PA 19107

(215) 955-1234
(215) 955-1390 fax

Medical School

Shiraz University


Hospital of University of Pennsylvania (HUP)


Hospital of University of Pennsylvania (HUP)

Board Certification


Hospital Appointment

Thomas Jefferson University Hospital
Methodist Hospital Division of Thomas Jefferson University Hospital

Research & Clinical Interests

My research focuses on...
Multiple Sclerosis is an autoimmune disease of the central nervous system that affects over 400,000 Americans and over 2 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:

1) 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.

2) 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.

3) 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."


Most Recent Peer-Reviewed Publications

  1. DAB389IL-2 recombinant fusion toxin effect on lymphocyte- and macrophage-producing cytokine subpopulation cells in experimentally induced demyelinating disease in mice
  2. Induction of peripheral tolerance in ongoing autoimmune inflammation requires interleukin 27 signaling in dendritic cells
  3. LPS-treated bone marrow-derived dendritic cells induce immune tolerance through modulating differentiation of CD4+regulatory T cell subpopulations mediated by 3G11 and CD127
  4. 1,25-Dihydroxyvitamin D3suppressed experimental autoimmune encephalomyelitis through both immunomodulation and oligodendrocyte maturation
  5. Prevalence of multiple sclerosis in Iranian emigrants: review of the evidence
  6. Selective depletion of CD11c+CD11b+dendritic cells partially abrogates tolerogenic effects of intravenous MOG in murine EAE
  7. Galectin-1 is essential for the induction of MOG35–55-based intravenous tolerance in experimental autoimmune encephalomyelitis
  8. IL-12Rβ2 has a protective role in relapsing-remitting experimental autoimmune encephalomyelitis
  9. Apoptotic cell-treated dendritic cells induce immune tolerance by specifically inhibiting development of CD4+effector memory T cells
  10. IL-9 signaling affects central nervous system resident cells during inflammatory stimuli
  11. Emerging immunopharmacological targets in multiple sclerosis
  12. 1,25-Dihydroxyvitamin D3 enhances neural stem cell proliferation and oligodendrocyte differentiation
  13. Analysis of 13 cell types reveals evidence for the expression of numerous novel primate- And tissue-specific microRNAs
  14. c-kit plays a critical role in induction of intravenous tolerance in experimental autoimmune encephalomyelitis
  15. Mechanisms of immunological tolerance in central nervous system inflammatory demyelination
  16. Granulocyte-macrophage colony-stimulating factor in central nervous system autoimmunity
  17. Expression of GM-CSF in T cells is increased in multiple sclerosis and suppressed by IFN-β therapy
  18. Silencing IFN-γ binding/signaling in astrocytes versus microglia leads to opposite effects on central nervous system autoimmunity
  19. Astrocyte-derived lactosylceramide implicated in multiple sclerosis
  20. Interferon regulatory factor (IRF) 3 is critical for the development of experimental autoimmune encephalomyelitis