Isolation of myeloid-derived suppressor cells (MDSC) from endometriotic mice model and their immunomodulatory functions
Methods in Cell Biology, ISSN: 0091-679X, Vol: 184, Page: 33-57
2024
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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
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Article Description
Endometriosis is a chronic, painful disease whose etiology remains unknown. The development of novel therapies and diagnostic tools for endometriosis has been limited due in part to challenges in studying the disease. Recently, a few reports have shown that immunosuppressive cells, such as myeloid-derived suppressor cell (MDSC), may promote the progression of endometriosis. MDSCs are a heterogeneous group of myeloid cells with potent immunosuppressive and angiogenic properties. Here, in this chapter, we provide a detailed protocol to phenotype MDSC as well as to isolate and assess the functionality from the peritoneal cavity of a mouse model of surgically induced endometriosis. Importantly, the current mouse model has been widely used to study how the immune system, hormones, and environmental factors affect endometriosis as well as the effects of endometriosis on fertility and pain.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0091679X23000857; http://dx.doi.org/10.1016/bs.mcb.2023.04.004; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85174462932&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/38555157; https://linkinghub.elsevier.com/retrieve/pii/S0091679X23000857; https://dx.doi.org/10.1016/bs.mcb.2023.04.004
Elsevier BV
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