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George Prendergast on Muck Rack

George Prendergast

  • President and CEO, Lankenau Institute for Medical Research
Philadelphia
As seen in: Nature, PLOS, Frontiers, Cell Press, The Journal of Immunology
Cancer research and other biomedical research
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Articles

Dietary L-Tryptophan consumption determines the number of colonic regulatory T cells and susceptibility to colitis via GPR15 - Nature Communications

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By Rachel M. Wigmore, Anne Kennedy, Carolina R. DaSilva, Jialing Huang, Gerald J. O’Connor, Miao Cao, Adam Snook, Michael Platten, Luis J. Sigal, George Prendergast
| Nature Verified
Abstract Environmental factors are the major contributor to the onset of immunological disorders such as ulcerative colitis. However, their identities remain unclear. Here, we discover that the amount of consumed L-Tryptophan (L-Trp), a ubiquitous dietary component, determines the transcription level of the colonic T cell homing receptor, GPR15, hence affecting the number of colonic FOXP3+ regulatory T (Treg) cells and local immune homeostasis.
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Gut-brain connections in neurodegenerative disease: immunotherapeutic targeting of Bin1 in inflammatory bowel disease and Alzheimer’s disease

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By Diego Iacono, Giuseppina Cantarella, George Prendergast
| Frontiers
Sunil Thomas* and George C. Prendergast Lankenau Institute for Medical Research, Wynnewood, PA, United States Longer lifespan produces risks of age-associated neurodegenerative disorders such as Alzheimer’s disease (AD), which is characterized by declines in memory and cognitive function.
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Bin1 targeted immunotherapy alters the status of the enteric neurons and the microbiome during ulcerative colitis treatment

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By Sunil Thomas, Giancarlo Mercogliano, George Prendergast
| PLOS
Changes in the microbiome after induction of UC It has been demonstrated that germ-free mice have an immature ENS that is normalized upon colonization with a normal microbiota. Communication between the microbiota and enteric neurons initiate serotonin release and activation of the serotonin (5-HT4) receptor. The interaction between the dysbiotic microbiota and ENS may lead to gastrointestinal disorders [19]. UC etiology is not understood.
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