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Shohreh Issazadeh

Researcher at Brigham and Women's Hospital

Publications -  9
Citations -  1030

Shohreh Issazadeh is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Experimental autoimmune encephalomyelitis & T cell. The author has an hindex of 9, co-authored 9 publications receiving 1013 citations. Previous affiliations of Shohreh Issazadeh include Harvard University.

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Nasal administration of amyloid‐β peptide decreases cerebral amyloid burden in a mouse model of Alzheimer's disease

TL;DR: It is demonstrated that chronic nasal administration of Aβ peptide can induce an immune response to Aβ that decreases cerebral Aβ deposition, suggesting a novel mucosal immunological approach for the treatment and prevention of AD.
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Elevated interleukin-12 in progressive multiple sclerosis correlates with disease activity and is normalized by pulse cyclophosphamide therapy

TL;DR: A Th1-type cytokine bias in peripheral blood mononuclear cells of untreated progressive MS patients that is reversed by CY/MP treatment and is associated with Th2 and TGF-beta (Th3) type responses is demonstrated.
Journal Article

Kinetics of Expression of Costimulatory Molecules and Their Ligands in Murine Relapsing Experimental Autoimmune Encephalomyelitis In Vivo

TL;DR: The kinetics of expression of costimulatory molecules and cytokines in the central nervous system in murine relapsing experimental autoimmune encephalomyelitis model characterized by remissions and relapses suggest that the targeting of costIMulatory molecules to block an immune response must take into account the expression patterns in the target organ.
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The role of CD154-CD40 versus CD28-B7 costimulatory pathways in regulating allogeneic Th1 and Th2 responses in vivo

TL;DR: Novel data indicate that Th1 and Th2 cells are differentially regulated by CD28-B7 versus CD154-CD40 costimulation pathways in vivo and may have potential implications for the development of therapeutic strategies such as T-cell costimulatory blockade in humans.
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Costimulatory signal blockade in murine relapsing experimental autoimmune encephalomyelitis

TL;DR: It is shown that administration of either MR1 (to block CD40L-CD40 T cell costimulatory signals) after immunization or after the first attack protects from EAE, and treatment with a combination of CTLA4Ig and MR1 provides additive protection.