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Arthur A. Vandenbark

Researcher at Oregon Health & Science University

Publications -  134
Citations -  7372

Arthur A. Vandenbark is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: Experimental autoimmune encephalomyelitis & T cell. The author has an hindex of 41, co-authored 134 publications receiving 6920 citations. Previous affiliations of Arthur A. Vandenbark include Veterans Health Administration & United States Department of Veterans Affairs.

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Middle-Age Male Mice Have Increased Severity of Experimental Autoimmune Encephalomyelitis and Are Unresponsive to Testosterone Therapy

TL;DR: Striking differences between middle-age vs young C57BL/6 male mice in the clinical course of EAE and response to both testosterone (T4) and estrogen (E2) hormone therapy are demonstrated, the first to define age-dependent differences in EAE expression and Response to hormone therapy.
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Treatment of experimental stroke with IL-10-producing B-cells reduces infarct size and peripheral and CNS inflammation in wild-type B-cell-sufficient mice.

TL;DR: These studies are the first to demonstrate a major immunoregulatory role for IL-10+ regulatory B-cells in preventing and treating MCAO in WT mice and also implicating their potential role in attenuating complications due to post-stroke immunosuppression.
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Phenotypic Changes in Immune Cell Subsets Reflect Increased Infarct Volume in Male vs. Female Mice

TL;DR: It is observed that males have a greater percentage of activated macrophages/microglia in the brain than females, as well as increased expression of the VLA-4 adhesion molecule in both brain and spleen, implying that effective treatments for human stroke may also be gender specific.
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T lymphocytes do not directly mediate the protective effect of estrogen on experimental autoimmune encephalomyelitis

TL;DR: It is shown that estrogen receptor-alpha (Esr1) is crucial for the protective effect of 17 beta-estradiol (E2) in murine experimental autoimmune encephalitis (EAE), an animal model of multiple sclerosis, and the first demonstration that the Protective effect of E2 on EAE is not mediated directly through E2-responsive T cells is provided.
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Evaluation of the Effects of 17β-Estradiol (17β-E2) on Gene Expression in Experimental Autoimmune Encephalomyelitis Using DNA Microarray

TL;DR: The results implicate a limited set of known and previously unsuspected E2-sensitive genes that may be crucial for inhibition of EAE and potentially the human disease, multiple sclerosis.