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Alternative activation of macrophages by filarial nematodes is MyD88-independent

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, MyD8...

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Detalles Bibliográficos
Autores principales: Mylonas, Katie J., Hoeve, Marieke A., MacDonald, Andrew S., Allen, Judith E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3608026/
https://www.ncbi.nlm.nih.gov/pubmed/22884360
http://dx.doi.org/10.1016/j.imbio.2012.07.006
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author Mylonas, Katie J.
Hoeve, Marieke A.
MacDonald, Andrew S.
Allen, Judith E.
author_facet Mylonas, Katie J.
Hoeve, Marieke A.
MacDonald, Andrew S.
Allen, Judith E.
author_sort Mylonas, Katie J.
collection PubMed
description 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.
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spelling pubmed-36080262013-04-05 Alternative activation of macrophages by filarial nematodes is MyD88-independent Mylonas, Katie J. Hoeve, Marieke A. MacDonald, Andrew S. Allen, Judith E. Immunobiology Article 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. Elsevier 2013-04 /pmc/articles/PMC3608026/ /pubmed/22884360 http://dx.doi.org/10.1016/j.imbio.2012.07.006 Text en © 2013 Elsevier GmbH. https://creativecommons.org/licenses/by/3.0/ Open Access under CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/) license
spellingShingle Article
Mylonas, Katie J.
Hoeve, Marieke A.
MacDonald, Andrew S.
Allen, Judith E.
Alternative activation of macrophages by filarial nematodes is MyD88-independent
title Alternative activation of macrophages by filarial nematodes is MyD88-independent
title_full Alternative activation of macrophages by filarial nematodes is MyD88-independent
title_fullStr Alternative activation of macrophages by filarial nematodes is MyD88-independent
title_full_unstemmed Alternative activation of macrophages by filarial nematodes is MyD88-independent
title_short Alternative activation of macrophages by filarial nematodes is MyD88-independent
title_sort alternative activation of macrophages by filarial nematodes is myd88-independent
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3608026/
https://www.ncbi.nlm.nih.gov/pubmed/22884360
http://dx.doi.org/10.1016/j.imbio.2012.07.006
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