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Hsing-Chuan Tsai

Researcher at Stanford University

Publications -  11
Citations -  408

Hsing-Chuan Tsai is an academic researcher from Stanford University. The author has contributed to research in topics: Neuroinflammation & Experimental autoimmune encephalomyelitis. The author has an hindex of 7, co-authored 11 publications receiving 239 citations. Previous affiliations of Hsing-Chuan Tsai include University of California, Davis.

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Journal ArticleDOI

Sphingosine-1-Phosphate (S1P) and S1P Signaling Pathway: Therapeutic Targets in Autoimmunity and Inflammation.

TL;DR: FTY720 (fingolimod), a non-selective S1PR modulator, significantly decreased annualized relapse rates in relapsing-remitting multiple sclerosis (MS), and recent studies suggest that FTY720 also decreases astrogliosis and promotes oligodendrocyte differentiation within the CNS and may have therapeutic benefit to prevent brain atrophy.
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IL-17A and Th17 Cells in Lung Inflammation: An Update on the Role of Th17 Cell Differentiation and IL-17R Signaling in Host Defense against Infection

TL;DR: Recent advances in unraveling the mechanism behind Th17 cell differentiation, IL-17A/IL-17R signaling, and also the importance of IL- 17A in pulmonary infection are summarized.
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Pericytes regulate vascular immune homeostasis in the CNS.

TL;DR: This paper showed that pericytes regulate the development of organ-specific characteristics of the brain vasculature such as the blood-brain barrier (BBB) and astrocytic end-feet and showed that myelin peptide-specific peripheral T cells in Pdgfb ret/ret ;2D2 tg mice lead to the development spontaneous neurological symptoms paralleled by the massive influx of leukocytes into the brain.
Posted ContentDOI

Pericytes regulate vascular immune homeostasis in the CNS

TL;DR: It is shown that pericytes indirectly restrict immune cell transmigration into the CNS under homeostatic conditions and during autoimmune-driven neuroinflammation by inducing immune quiescence of brain endothelial cells.
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Effects of sphingosine-1-phosphate receptor 1 phosphorylation in response to FTY720 during neuroinflammation.

TL;DR: It is found that mice carrying a phosphorylation-defective S1pr1 gene [S1PR1(S5A) mice] were refractory to FTY720 treatment in MOG35-55-immunized and Th17-mediated experimental autoimmune encephalomyelitis (EAE) models, suggesting that cell type-specific therapies may enhance therapeutic efficacy in MS.