Control of Th2-Mediated Inflammation by Regulatory T Cells
The American Journal of Pathology, ISSN: 0002-9440, Vol: 177, Issue: 2, Page: 525-531
2010
- 55Citations
- 68Captures
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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.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations55
- Citation Indexes55
- 55
- CrossRef51
- Captures68
- Readers68
- 68
Review Description
Allergic diseases and asthma are caused by dysregulated Th2-type immune responses, which drive disease development in susceptible individuals. Immune tolerance to allergens prevents inflammatory symptoms in the respiratory mucosa and provides protection against inflammation in the airways. Increasing evidence indicates that Foxp3+ regulatory T cells (Tregs) play a critical role in immune tolerance and control Th2-biased responses. Tregs develop in the thymus from CD4 + T cells (natural Tregs) and also in the periphery by the conversion of naïve CD4 + T cells (induced Tregs). Increased susceptibility to allergy and airway inflammation is hypothesized to result from impaired development and function of Tregs. Thus, strategies to induce allergen-specific Tregs hold great promise for treatment and prevention of asthma.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0002944010601083; http://dx.doi.org/10.2353/ajpath.2010.090936; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=77957273661&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/20566752; https://linkinghub.elsevier.com/retrieve/pii/S0002944010601083
Elsevier BV
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