Catálogo de publicaciones - revistas

<jats:title>Allergy Induction</jats:title> <jats:p> Proteinases found in fungi and other allergens elicit allergic inflammation, but how they do so is far from clear. It is also unclear how pattern recognition receptors, which detect invading microbes, drive allergic inflammation. <jats:bold> Millien <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6147" page="792" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1240342">792</jats:related-article> ) shed light on this puzzle by showing that, in mice, induction of allergic inflammation requires proteinase-dependent cleavage of the clotting factor fibrinogen, leading to generation of a ligand that activates the pattern-recognition receptor, Toll-like receptor 4 (TLR4). Cleaved fibrinogen signals through TLR4 to activate the innate immune system and recruit cells to the airway, which drives both allergic responses and antifungal immunity. </jats:p>

<jats:title>Insect Cycles</jats:title> <jats:p> Rapid increases in insect populatio n sizes can result in significant crop losses. Seasonal temperature has been proposed to drive such outbreaks. Despite clear evidence that temperature can drive individual insect development, its influence at the population level is much less clear. <jats:bold> Nelson <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6147" page="796" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1238477">796</jats:related-article> , published online 1 August) analyzed data collected over 50 years on the tea tortrix moth, which affects Japanese tea plantations, to reveal the impacts of temperature on cyclical outbreaks. </jats:p>

<jats:title>Food as Reward</jats:title> <jats:p> Why does ice cream taste so good? High-fat foods activate a reward circuit in the brain involving dopamine, a neurotransmitter that regulates pleasure. Overconsumption of high-fat foods is thought to dampen this dopamine-induced reward sensation, leading to compensatory consumption of even more high-fat foods. The mechanisms by which dietary fat in the gut “talks” to the dopamine reward circuit are unclear. <jats:bold> Tellez <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6147" page="800" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1239275">800</jats:related-article> ) suggest that an intestinal lipid messenger called oleoylethanolamine (OEA) may play a role—at least in mice. Mice on a high-fat diet had unusually low levels of intestinal OEA and exhibited deficient dopaminergic responses to gut stimulation with high-fat lipids. Infusion of OEA into these mice restored the dopaminergic response, and mice that had been accustomed to a high-fat diet began to eat more low-fat foods. </jats:p>

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<jats:title>Next-Generation Gene Therapy</jats:title> <jats:p> Few disciplines in contemporary clinical research have experienced the high expectations directed at the gene therapy field. However, gene therapy has been challenging to translate to the clinic, often because the therapeutic gene is expressed at insufficient levels in the patient or because the gene delivery vector integrates near protooncogenes, which can cause leukemia (see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6148" page="853" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1242551">Verma</jats:related-article> </jats:bold> ). <jats:bold> Biffi <jats:italic>et al.</jats:italic> </jats:bold> ( <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://www.sciencemag.org/content/341/6148/1233158.full">1233158</jats:ext-link> , published online 11 July) and <jats:bold> Aiuti <jats:italic>et al.</jats:italic> </jats:bold> ( <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://www.sciencemag.org/content/341/6148/1233151.full">1233151</jats:ext-link> ; published online 11 July) report progress on both fronts in gene therapy trials of three patients with metachromatic leukodystrophy (MLD), a neurodegenerative disorder, and three patients with Wiskott-Aldrich syndrome (WAS), an immunodeficiency disorder. Optimized lentiviral vectors were used to introduce functional <jats:italic>MLD</jats:italic> or <jats:italic>WAS</jats:italic> genes into the patients' hematopoietic stem cells (HSCs) ex vivo, and the transduced cells were then infused back into the patients, who were then monitored for up to 2 years. In both trials, the patients showed stable engraftment of the transduced HSC and high expression levels of functional <jats:italic>MLD</jats:italic> or <jats:italic>WAS</jats:italic> genes. Encouragingly, there was no evidence of lentiviral vector integration near proto-oncogenes, and the gene therapy treatment halted disease progression in most patients. A longer follow-up period will be needed to further validate efficacy and safety. </jats:p>

<jats:title>Next-Generation Gene Therapy</jats:title> <jats:p> Few disciplines in contemporary clinical research have experienced the high expectations directed at the gene therapy field. However, gene therapy has been challenging to translate to the clinic, often because the therapeutic gene is expressed at insufficient levels in the patient or because the gene delivery vector integrates near protooncogenes, which can cause leukemia (see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6148" page="853" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1242551">Verma</jats:related-article> </jats:bold> ). <jats:bold> Biffi <jats:italic>et al.</jats:italic> </jats:bold> ( <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://www.sciencemag.org/content/341/6148/1233158.full">1233158</jats:ext-link> , published online 11 July) and <jats:bold> Aiuti <jats:italic>et al.</jats:italic> </jats:bold> ( <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://www.sciencemag.org/content/341/6148/1233151.full">1233151</jats:ext-link> ; published online 11 July) report progress on both fronts in gene therapy trials of three patients with metachromatic leukodystrophy (MLD), a neurodegenerative disorder, and three patients with Wiskott-Aldrich syndrome (WAS), an immunodeficiency disorder. Optimized lentiviral vectors were used to introduce functional <jats:italic>MLD</jats:italic> or <jats:italic>WAS</jats:italic> genes into the patients' hematopoietic stem cells (HSCs) ex vivo, and the transduced cells were then infused back into the patients, who were then monitored for up to 2 years. In both trials, the patients showed stable engraftment of the transduced HSC and high expression levels of functional <jats:italic>MLD</jats:italic> or <jats:italic>WAS</jats:italic> genes. Encouragingly, there was no evidence of lentiviral vector integration near proto-oncogenes, and the gene therapy treatment halted disease progression in most patients. A longer follow-up period will be needed to further validate efficacy and safety. </jats:p>