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• W2008945707 abstract "Clinical asthma is very widely assumed to be the net result of excessive inflammation driven by aberrant T-helper-2 (Th2) immunity that leads to inflamed, remodelled airways and then functional derangement that, in turn, causes symptoms. This notion of disease is actually poorly supported by data, and there are substantial discrepancies and very poor correlation between inflammation, damage, functional impairment, and degree of symptoms. Furthermore, this problem is compounded by the poor understanding of the heterogeneity of clinical disease. Failure to recognise and discover the underlying mechanisms of these major variants or endotypes of asthma is, arguably, the major intellectual limitation to progress at present. Fortunately, both clinical research and animal models are very well suited to dissecting the cellular and molecular basis of disease endotypes. This approach is already suggesting entirely novel pathways to disease—eg, alternative macrophage specification, steroid refractory innate immunity, the interleukin-17–regulatory T-cell axis, epidermal growth factor receptor co-amplification, and Th2-mimicking but non-T-cell, interleukins 18 and 33 dependent processes that can offer unexpected therapeutic opportunities for specific patient endotypes. Clinical asthma is very widely assumed to be the net result of excessive inflammation driven by aberrant T-helper-2 (Th2) immunity that leads to inflamed, remodelled airways and then functional derangement that, in turn, causes symptoms. This notion of disease is actually poorly supported by data, and there are substantial discrepancies and very poor correlation between inflammation, damage, functional impairment, and degree of symptoms. Furthermore, this problem is compounded by the poor understanding of the heterogeneity of clinical disease. Failure to recognise and discover the underlying mechanisms of these major variants or endotypes of asthma is, arguably, the major intellectual limitation to progress at present. Fortunately, both clinical research and animal models are very well suited to dissecting the cellular and molecular basis of disease endotypes. This approach is already suggesting entirely novel pathways to disease—eg, alternative macrophage specification, steroid refractory innate immunity, the interleukin-17–regulatory T-cell axis, epidermal growth factor receptor co-amplification, and Th2-mimicking but non-T-cell, interleukins 18 and 33 dependent processes that can offer unexpected therapeutic opportunities for specific patient endotypes. Asthma: still more questions than answersAs we did in 2006, we are dedicating this week's issue to asthma to coincide with the European Respiratory Society meeting to be held in Berlin, Oct 4–8. In collaboration with the Society, The Lancet is hosting a hot-topic session at the conference that discusses new targets for drug development, insights into the use of inflammatory markers, new understanding of the complexity of disease progression and exacerbation, and new concepts of pathogenic mechanisms. So how much progress has been made in the understanding, treatment, and prevention of asthma? Despite intense epidemiological and basic research, three fundamental questions remain tantalisingly puzzling. Full-Text PDF" @default.
• W2008945707 created "2016-06-24" @default.
• W2008945707 creator A5008084743 @default.
• W2008945707 date "2008-09-01" @default.
• W2008945707 modified "2023-10-16" @default.
• W2008945707 title "Endotyping asthma: new insights into key pathogenic mechanisms in a complex, heterogeneous disease" @default.
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