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Farinaz Safavi

Researcher at Thomas Jefferson University

Publications -  32
Citations -  1765

Farinaz Safavi is an academic researcher from Thomas Jefferson University. The author has contributed to research in topics: Experimental autoimmune encephalomyelitis & Medicine. The author has an hindex of 11, co-authored 25 publications receiving 1329 citations. Previous affiliations of Farinaz Safavi include SUNY Downstate Medical Center & King's College London.

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The encephalitogenicity of T(H)17 cells is dependent on IL-1- and IL-23-induced production of the cytokine GM-CSF.

TL;DR: Cross-regulation of IL-23 and GM- CSF explains the similar pattern of resistance to autoimmunity when either of the two cytokines is absent and identifies TH17 cells as a crucial source of GM-CSF in autoimmune inflammation.
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B-cell depleting therapies may affect susceptibility to acute respiratory illness among patients with multiple sclerosis during the early COVID-19 epidemic in Iran.

TL;DR: Whether the course of COVID-19 is more severe in patients with MS and if MS disease-modifying treatments (DMTs) affect the risk of contracting the disease is determined and B-cell depleting antibodies may increase the susceptibility to contracting CO VID-19.
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Expression of GM-CSF in T Cells Is Increased in Multiple Sclerosis and Suppressed by IFN-β Therapy

TL;DR: To characterize GM-CSF production by T cells of MS patients and to determine the effect of IFN-β therapy on its production, a potential mechanism ofIFN- β therapy, namely suppression of GM- CSF production is revealed.
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Role of serine proteases in inflammation: Bowman–Birk protease inhibitor (BBI) as a potential therapy for autoimmune diseases

TL;DR: The Bowman-Birk protease inhibitor (BBI), a soybean-derived serine protease inhibitors, is resistant to temperature and acidic conditions, which makes it a good candidate for oral administration, with no major side effects.
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Neurovascular injury with complement activation and inflammation in COVID-19

TL;DR: Antibody-mediated cytotoxicity directed against the endothelial cells is the most likely initiating event that leads to vascular leakage, platelet aggregation, neuroinflammation and neuronal injury in patients with coronavirus disease 2019.