Regulatory t-cell control of type 2 inflammation
The Th2 Type Immune Response in Health and Disease: From Host Defense and Allergy to Metabolic Homeostasis and Beyond, Page: 73-95
2015
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Book Chapter Description
Regulatory T cells (Tregs) are a physiological, and potent, means of repressing immune responsiveness by acting on a range of cell types, most notably T cells, dendritic cells, and macrophages, neutralizing their function or recruiting them into the regulatory network. Tregs play a vital role in maintaining body health and homeostasis in the constant presence of commensal organisms and environmental antigens, but they also need to step aside when infection or other threats are faced. The delicate balance between restraint and response is not infrequently misjudged by the immune system, leading to immunopathological syndromes in the case of deficient Treg function, or progressive disease from infection or cancer where Tregs are overactive. This relationship is amply illustrated in regulation of the Th2 response, in which excessive reactivity to harmless exogenous molecules (allergens) gives rise to allergic diseases, while susceptibility to a range of parasites reflects a suppressed Th2 immunity to infection. Understanding the broader role of Tregs in controlling both Th2-mediated immunopathologies and Th2-dependent immunity is therefore key to developing new strategies to treat both allergic disorders and chronic parasite infections
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84978259282&origin=inward; http://dx.doi.org/10.1007/978-1-4939-2911-5_5; https://link.springer.com/10.1007/978-1-4939-2911-5_5; https://dx.doi.org/10.1007/978-1-4939-2911-5_5; https://link.springer.com/chapter/10.1007/978-1-4939-2911-5_5
Springer Science and Business Media LLC
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