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Wayne W. Hancock

Researcher at Children's Hospital of Philadelphia

Publications -  509
Citations -  37752

Wayne W. Hancock is an academic researcher from Children's Hospital of Philadelphia. The author has contributed to research in topics: Transplantation & FOXP3. The author has an hindex of 103, co-authored 505 publications receiving 35694 citations. Previous affiliations of Wayne W. Hancock include Boston University & Takeda Pharmaceutical Company.

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Fibrinogen Stimulates Macrophage Chemokine Secretion Through Toll-Like Receptor 4

TL;DR: It is suggested that innate responses to fibrinogen and bacterial endotoxin may converge at the evolutionarily conserved Toll-like recognition molecules, thereby promoting immune surveillance at sites of inflammation.
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CCR5+ and CXCR3+ T cells are increased in multiple sclerosis and their ligands MIP-1α and IP-10 are expressed in demyelinating brain lesions

TL;DR: Findings provide a rationale for the use of agents that block CCR5 and/or CXCR3 as a therapeutic approach in the treatment of MS and potentially for other chronic autoimmune/inflammatory processes such as rheumatoid arthritis, autoimmune diabetes, or chronic transplant rejection.
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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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Oral tolerance to myelin basic protein and natural recovery from experimental autoimmune encephalomyelitis are associated with downregulation of inflammatory cytokines and differential upregulation of transforming growth factor beta, interleukin 4, and prostaglandin E expression in the brain.

TL;DR: In this paper, the authors investigated the effect of myelin basic protein (MBP) injection on the severity of EAE in the Lewis rat and found that oral tolerance to MBP is enhanced by the concomitant oral administration of lipopolysaccharide (LPS).
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Foxp3 Reprograms T Cell Metabolism to Function in Low-Glucose, High-Lactate Environments

TL;DR: It is reported that the Treg transcription factor Foxp3 reprograms T cell metabolism by suppressing Myc and glycolysis, enhancing oxidative phosphorylation, and increasing nicotinamide adenine dinucleotide oxidation, which allows Tregs a metabolic advantage in low-glucose, lactate-rich environments.