Abstract:
:Alternative macrophage activation is largely defined by IL-4Rα stimulation but the contribution of Toll-like receptor (TLR) signaling to this phenotype is not currently known. We have investigated macrophage activation status under Th2 conditions in the absence of the core TLR adaptor molecule, MyD88. No impairment was observed in the ability of MyD88-deficient bone marrow derived macrophages to produce or express alternative activation markers, including arginase, RELM-α or Ym1, in response to IL-4 treatment in vitro. Further, we observed no difference in the ability of peritoneal exudate cells from nematode implanted wild type (WT) or MyD88-deficient mice to produce arginase or express the alternative activation markers RELM-α or Ym1. Therefore, MyD88 is not a fundamental requirement for Th2-driven macrophage alternative activation, either in vitro or in vivo.
journal_name
Immunobiologyjournal_title
Immunobiologyauthors
Mylonas KJ,Hoeve MA,MacDonald AS,Allen JEdoi
10.1016/j.imbio.2012.07.006subject
Has Abstractpub_date
2013-04-01 00:00:00pages
570-8issue
4eissn
0171-2985issn
1878-3279pii
S0171-2985(12)00170-2journal_volume
218pub_type
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