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Andrew D. Wells

Researcher at Children's Hospital of Philadelphia

Publications -  148
Citations -  12602

Andrew D. Wells is an academic researcher from Children's Hospital of Philadelphia. The author has contributed to research in topics: T cell & Genome-wide association study. The author has an hindex of 47, co-authored 130 publications receiving 10250 citations. Previous affiliations of Andrew D. Wells include University of Wisconsin-Madison & University of New Mexico.

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Drug repurposing: progress, challenges and recommendations

TL;DR: Approaches used for drug repurposing (also known as drug repositioning) are presented, the challenges faced by the repurpose community are discussed, and innovative ways by which these challenges could be addressed are recommended to help realize the full potential of drugRepurposing.
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Deacetylase inhibition promotes the generation and function of regulatory T cells

TL;DR: Administration of an HDAC inhibitor (HDACi) in vivo increased Foxp3 gene expression, as well as the production and suppressive function of regulatory T cells (Treg cells), and HDAC9 proved particularly important in regulatingFoxp3-dependent suppression.
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Blocking both signal 1 and signal 2 of T-cell activation prevents apoptosis of alloreactive T cells and induction of peripheral allograft tolerance

TL;DR: The data indicate that induction of T-cell apoptosis and peripheral allograft tolerance is prevented by blocking both signal 1 and signal 2 ofT-cell activation.
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Requirement for T-cell apoptosis in the induction of peripheral transplantation tolerance.

TL;DR: It is found that mice with defective passive or active T-cell apoptotic pathways were resistant to induction of transplantation tolerance, and deletion of activated T cells through activation-induced cell death or growth factor withdrawal seems necessary to achieve peripheral tolerance across major histocompatibility complex barriers.
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Quantifying the frequency of alloreactive T cells in vivo: new answers to an old question.

TL;DR: It is concluded that accurate calculations of alloreactive precursor frequency must account for both proliferation and cell engraftment, and that bystander proliferation is negligible, revealing exquisite specificity to the alloresponse.