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Jesús Amo-Aparicio

Researcher at Autonomous University of Barcelona

Publications -  13
Citations -  310

Jesús Amo-Aparicio is an academic researcher from Autonomous University of Barcelona. The author has contributed to research in topics: Inflammation & Neuroprotection. The author has an hindex of 6, co-authored 8 publications receiving 190 citations.

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IL-4 drives microglia and macrophages toward a phenotype conducive for tissue repair and functional recovery after spinal cord injury.

TL;DR: It is shown that IL‐4 protein levels are undetectable in the spinal cord after contusion injury, which likely favors microglia and macrophages to remain in a pro‐inflammatory state, and that therapies aimed at increasing IL-4 levels could be valuable for the treatment of acute SCI.
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Role for nuclear interleukin-37 in the suppression of innate immunity

TL;DR: In this article, the role of nuclear IL-37 remains unknown on the ability of this cytokine to inhibit innate inflammation and acquired immunity, but it has been shown that IL37 is a dual function cytokine in that it not only translocates to the nucleus but also transmits a signal via surface membrane receptors.
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BET protein inhibition regulates cytokine production and promotes neuroprotection after spinal cord injury

TL;DR: BET protein inhibition is an effective treatment to regulate cytokine production and promote neuroprotection after SCI and is demonstrated for the first time that targeting BET proteins is an encouraging approach for SCI repair and a potential strategy to treat other inflammatory pathologies.
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CD200 modulates spinal cord injury neuroinflammation and outcome through CD200R1.

TL;DR: Interaction of CD200-CD200R1 plays a crucial role in limiting inflammation and lesion progression after SCI, and that boosting the stimulation of this pathway may constitute a new therapeutic approach.
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IL-37 exerts therapeutic effects in experimental autoimmune encephalomyelitis through the receptor complex IL-1R5/IL-1R8

TL;DR: It is demonstrated that IL-37 reduces inflammation and protects against neurological deficits and myelin loss in EAE mice by acting via IL1-R5/IL1- R8, and that this protective physiological mechanism is defective in MS individuals.