E
Edward J. Pearce
Researcher at Max Planck Society
Publications - 237
Citations - 34759
Edward J. Pearce is an academic researcher from Max Planck Society. The author has contributed to research in topics: Schistosoma mansoni & Immune system. The author has an hindex of 81, co-authored 218 publications receiving 30184 citations. Previous affiliations of Edward J. Pearce include National Institutes of Health & Ithaca College.
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Journal ArticleDOI
Human Transforming Growth Factor-β Activates a Receptor Serine/Threonine Kinase from the Intravascular ParasiteSchistosoma mansoni
TL;DR: TGF-β is implicate as a ligand for SmRK1 and as a potential host-derived regulator of parasite growth and development.
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Immunometabolism in 2017: Driving immunity: all roads lead to metabolism.
Edward J. Pearce,Erika L. Pearce +1 more
TL;DR: In 2017, studies of cellular metabolism broadly permeated immunological research and accumulating data support the view that understanding how metabolism regulates immune cell function could provide new therapeutic opportunities for the many diseases associated with immune system dysregulation.
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IL-10R blockade during chronic schistosomiasis mansoni results in the loss of B cells from the liver and the development of severe pulmonary disease.
Keke C. Fairfax,Eyal Amiel,Irah L. King,Tori C. Freitas,Markus Mohrs,Edward J. Pearce,Edward J. Pearce +6 more
TL;DR: A role for IL-10-dependent B cell responses in the regulation of tissue damage during a chronic helminth infection is described.
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The human immune response to defined immunogens of Schistosoma mansoni: elevated antibody levels to paramyosin in stool-negative individuals from two endemic areas in Brazil
Rodrigo Correa-Oliveira,Edward J. Pearce,Guilherme Oliveira,Denise B. Golgher,Naftale Katz,L.G. Bahia,Omar dos Santos Carvalho,Giovanni Gazzinelli,Alan Sher +8 more
TL;DR: The results suggest that the immune response of humans to paramyosin may play a role in natural resistance to schistosome infection, and that an elevated antibody level against this antigen may be a useful correlate of drug-induced cure.
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Schistosomiasis delays lesion resolution during Leishmania major infection by impairing parasite killing by macrophages.
TL;DR: The results suggest that pre‐existence of a strong Th2 response‐dominated infection can alter the responses to Th1‐inducing pathogens at peripheral sites and impair Th1-mediated effector functions.