Journal article
The anti-inflammatory actions of IL-4 in human monocytes are not mediated by IL-10, RP105 or the kinase activity of RIPK2
EA Woodward, TB Kolesnik, SE Nicholson, CM Prêle, PH Hart
Cytokine | Published : 2012
Abstract
The anti-inflammatory actions of IL-4 in activated human monocytes may reflect transcriptional regulation of genes involved in TLR signaling pathways. Tailored gene arrays were conducted to profile the expression of 84 genes central to TLR-mediated signal transduction in human monocytes treated with the TLR4 ligand, LPS, with or without IL-4. In the first 3h, IL-4 down-regulated mRNA levels of LPS-induced inflammatory cytokines and chemokines, without altering mRNA levels of TLRs, TLR-related signaling molecules or multiple transcription factors. The down-regulation of inflammatory genes by IL-4 was preceded by an early up-regulation of IL-10 mRNA and protein and mRNA for receptor-interactin..
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Awarded by National Health and Medical Research Council
Funding Acknowledgements
We thank Dr. Mark Febbraio and Greg Kowalski from Baker IDI Heart and Diabetes Institute, Melbourne Australia, for supplying the IL10<SUP>-/-</SUP> mice and Dr. Michelle Tourigny for her expert advice on setting up and optimizing flow cytometry experiments. This work was supported by a National Health and Medical Research Council (NHMRC) of Australia Grant 275546 to P.H.H. and in part by NHMRC Program Grant 461219 and Victorian State Government Operational Infrastructure Support and Australian Government NHMRC IRIISS to S.E.N., E.A.W. was supported by a Murdoch University Research Studentship and a Stan and Jean Perron Scholarship awarded by the Telethon Institute for Child Health Research. C.M.P. was supported in part by AFA-ARA Heald Fellowship. S.E.N. and P.H.H. were supported by an NHMRC Fellowship.