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MyD88‐dependent production of IL‐17F is modulated by the anaphylatoxin C5a via the Akt signaling pathway
dc.contributor.authorBosmann, Markus
dc.contributor.authorPatel, Vinay R.
dc.contributor.authorRusskamp, Norman F.
dc.contributor.authorPache, Florence
dc.contributor.authorZetoune, Firas S.
dc.contributor.authorSarma, J. Vidya
dc.contributor.authorWard, Peter A.
dc.date.accessioned2020-03-17T18:29:16Z
dc.date.available2020-03-17T18:29:16Z
dc.date.issued2011-12
dc.identifier.citationBosmann, Markus; Patel, Vinay R.; Russkamp, Norman F.; Pache, Florence; Zetoune, Firas S.; Sarma, J. Vidya; Ward, Peter A. (2011). "MyD88‐dependent production of IL‐17F is modulated by the anaphylatoxin C5a via the Akt signaling pathway." The FASEB Journal 25(12): 4222-4232.
dc.identifier.issn0892-6638
dc.identifier.issn1530-6860
dc.identifier.urihttps://hdl.handle.net/2027.42/154335
dc.description.abstractThe interleukin‐17 (IL‐17) family of cytokines plays important roles in innate immune defenses against bacterial and fungal pathogens. While much is known about IL‐17A, much less information is available about the IL‐17F isoform. Here, we investigated gene expression and release of IL‐17F and its regulation by the complement system. IL‐17F was produced in mouse peritoneal elicited macrophages after TLR4 activation by LPS, peaking after 12 h. This effect was completely dependent on the presence of the adaptor protein MyD88. The copresence of the complement activation product, C5a (EC50=10 nM), amplified IL‐17F production via the receptor C5aR. In vitro signaling studies indicated that LPS or C5a, or the combination, caused phosphorylation of Akt occurring at threonine 308 but not at serine 473. Treatment of macrophages with pharmacologic inhibitors of PI3K‐Akt greatly reduced production of IL‐17F as well as mRNA for IL‐17F. In endotoxemia, C5a levels peaked at 6 h, while IL‐17F levels peaked between 6‐12 h. Full in vivo production of IL‐17F during endotoxemia required C5a. A similar result was found in the cecal ligation and puncture sepsis model. These data suggest that maximal production of IL‐17F requires complement activation and presence of C5a.—Bosmann, M., Patel, V. R., Russkamp, N. F., Pache, F., Zetoune, F. S., Sarma, J. V., Ward, P. A. MyD88‐dependent production of IL‐17F is modulated by the anaphylatoxin C5a via the Akt signaling pathway. FASEB J. 25, 4222–4232 (2011). www.fasebj.org
dc.publisherWiley Periodicals, Inc.
dc.subject.otherpolymicrobial sepsis
dc.subject.othermacrophages
dc.subject.otherKey Words
dc.subject.otherendotoxemia
dc.subject.otherendotoxic shock
dc.subject.othercecal ligation and puncture
dc.titleMyD88‐dependent production of IL‐17F is modulated by the anaphylatoxin C5a via the Akt signaling pathway
dc.typeArticle
dc.rights.robotsIndexNoFollow
dc.subject.hlbsecondlevelBiology
dc.subject.hlbtoplevelScience
dc.description.peerreviewedPeer Reviewed
dc.description.bitstreamurlhttps://deepblue.lib.umich.edu/bitstream/2027.42/154335/1/fsb2fj11191205.pdf
dc.identifier.doi10.1096/fj.11-191205
dc.identifier.sourceThe FASEB Journal
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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