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Matthew Lacorcia

Researcher at Technische Universität München

Publications -  8
Citations -  70

Matthew Lacorcia is an academic researcher from Technische Universität München. The author has contributed to research in topics: Immune system & Immunology. The author has an hindex of 3, co-authored 5 publications receiving 33 citations.

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Host immune responses during Taenia solium Neurocysticercosis infection and treatment.

TL;DR: The immunological parameters associated with NCC in people living with HIV/AIDS and treatments are discussed, and open questions to understand the role of the immune system and its impact in this intriguing host–parasite crosstalk are proposed.
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Maternal Schistosomiasis: Immunomodulatory Effects With Lasting Impact on Allergy and Vaccine Responses

TL;DR: This review explores how maternal schistosome infection could drive changes in immune system development of offspring and how this may lead to identifying factors involved in altering responses to vaccination as well as manifestations of immune disorders including allergy.
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Placental gene expression and antibody levels of mother-neonate pairs reveal an enhanced risk for inflammation in a helminth endemic country.

TL;DR: Exposure in utero to different environments alters placental gene expression and thus possibly plays a role in the development and modulation of the immune system of the offspring, demonstrating that exposure to environmental factors can modify the development of allergies later in life.
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Fetomaternal immune cross talk modifies T-cell priming through sustained changes to DC function.

TL;DR: In this paper, a model of chronic maternal schistosomiasis infection was combined with a thorough analysis of subsequent offspring immune responses to allergy and vaccination models, including viral challenge and steady-state changes to immune cell compartments.
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Helminthic dehydrogenase drives PGE2 and IL‐10 production in monocytes to potentiate Treg induction

TL;DR: It is shown that glutamate dehydrogenase from viable cysts instructs tolerogenic monocytes to release IL‐10 and the lipid mediator PGE2, and Harnessing the P GE2‐IL‐10 axis and targeting TGF‐ß signaling may offer an important therapeutic strategy in inflammatory epilepsy and NCC.