Identification of the salmonid IL-17A/F1a/b, IL-17A/F2b, IL-17A/F3 and IL-17N genes and analysis of their expression following in vitro stimulation and infection
Immunogenetics, ISSN: 1432-1211, Vol: 67, Issue: 7, Page: 395-412
2015
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- 33Captures
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Identification of the salmonid IL-17A/F1a/b, IL-17A/F2b, IL-17A/F3 and IL-17N genes and analysis of their expression following in vitro stimulation and infection.
Authors: Tiehui Wang, Yousheng Jiang, Alex Wang, Mansourah Husain, Qiaoqing Xu, Christopher J Secombes PMID: 25943775 DOI: 10.1007/s00251-015-0838-1 Publication Type: Research Support, Non-U.S. Gov’t ISSN:
Article Description
This study identifies four new IL-17A/F isoforms in salmonids, as well as IL-17N. IL-17A/F1 and IL-17A/F2 are each represented by two paralogues, with a predicted pseudogene of IL-17N also apparent in the salmonid genome. Analysis of the sequences and genes of the known IL-17A/F and IL-17N molecules suggests that IL-17N is a member within the IL-17A/F subfamily. Analysis of factors that modulated the expression of these genes showed that PHA and PMA were good inducers of salmon IL-17A/F1a and IL-17A/F2a, with rIL-21 a potent stimulator of IL-17A/F1a and IL-17A/F3. The potential involvement of these isoforms during responses post-vaccination and infection was also studied. In unvaccinated control fish, Yersinia ruckeri infection resulted in a marked up-regulation of IL-17A/F1a and IL-17N in the spleen and head kidney and IL-17A/F2a and IL-17A/F3 in the spleen. In the vaccinated fish, only one significant increase was seen relative to control fish, of IL-17A/F2a in the gills, whether the fish were challenged with Y. ruckeri or given the saline placebo. It was also apparent in the gills and head kidney that the level of IL-17A/F1b remained elevated in the Y. ruckeri-challenged fish at a time when it had decreased in saline-injected fish. The relative importance of these isoforms for disease resistance remains to be determined.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84930543114&origin=inward; http://dx.doi.org/10.1007/s00251-015-0838-1; http://www.ncbi.nlm.nih.gov/pubmed/25943775; http://link.springer.com/10.1007/s00251-015-0838-1; https://dx.doi.org/10.1007/s00251-015-0838-1; https://link.springer.com/article/10.1007/s00251-015-0838-1
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