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João H. Duarte

Researcher at National Institute for Medical Research

Publications -  58
Citations -  3351

João H. Duarte is an academic researcher from National Institute for Medical Research. The author has contributed to research in topics: Connective tissue & Immune system. The author has an hindex of 15, co-authored 56 publications receiving 2886 citations. Previous affiliations of João H. Duarte include University of Coimbra & Instituto Gulbenkian de Ciência.

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Fate mapping of IL-17-producing T cells in inflammatory responses

TL;DR: A reporter mouse strain designed to map the fate of cells that have activated interleukin 17A (IL-17A) allows the actual functional fate of effector T cells to be related to TH17 developmental origin regardless of IL-17 expression.
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The Aryl Hydrocarbon Receptor: Multitasking in the Immune System

TL;DR: The current understanding of the molecular interactions and functions of AhR in the immune system in steady state and in the presence of infection and inflammation is reviewed, with a focus on barrier organs such as the skin, the gut, and the lung.
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Plasticity of Th17 cells in Peyer's patches is responsible for the induction of T cell-dependent IgA responses.

TL;DR: It is found that endogenous cells of the TH17 subset of helper T cells in lymphoid organs of naive mice 'preferentially' homed to the intestines and were maintained independently of IL-23.
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Activation of the aryl hydrocarbon receptor dampens the severity of inflammatory skin conditions.

TL;DR: It is shown that the aryl hydrocarbon receptor (AhR), a transcription factor that senses environmental stimuli, modulates pathology in psoriasis and suggests a critical role for AhR in the regulation of inflammatory responses and opens the possibility for novel therapeutic strategies in chronic inflammatory disorders.
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Natural Treg cells spontaneously differentiate into pathogenic helper cells in lymphopenic conditions

TL;DR: The findings that Treg convert into pathogenic Th cells in absence of IL‐2 provide new clues to the success of Treg‐based immune therapies.