IL-13 induces the expression of the alternative activation marker Ym1 in a subset of testicular macrophages
Journal of Reproductive Immunology, ISSN: 0165-0378, Vol: 78, Issue: 2, Page: 140-148
2008
- 41Citations
- 52Captures
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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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Metrics Details
- Citations41
- Citation Indexes36
- 36
- CrossRef30
- Policy Citations5
- 5
- Captures52
- Readers52
- 52
Article Description
Macrophages are thought to play an important role in the maintenance of immune privilege in the testis, which functions to prevent immune responses to developing sperm. Two populations of macrophages are known to exist in the testis, one of which exhibits immunosuppressive activity. Macrophages that are alternatively activated with either IL-4 or IL-13 have been shown to be anti-inflammatory and promote wound healing. Expression of the Ym1 protein is an established marker of alternatively activated macrophages. Testicular macrophages were examined for expression of Ym1 protein, and it was found to be highly expressed in a subpopulation of CD11b + cells. Furthermore, we have shown that Ym1 protein expression in the testis is dependent upon IL-13R signaling, and that IL-13 is produced in the testis. These data suggest that IL-13 plays a role in testicular immune privilege by the maintenance of an alternatively activated macrophage population.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0165037808000041; http://dx.doi.org/10.1016/j.jri.2008.01.001; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=46549084100&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/18329106; https://linkinghub.elsevier.com/retrieve/pii/S0165037808000041
Elsevier BV
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