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Here, we analyzed M<\/jats:styled-content>s4a8a+<\/jats:sup> macrophages in M<\/jats:styled-content>2\u2010associated infectious pathologies. In late\u2010stage T<\/jats:styled-content>rypanosoma congolense<\/jats:italic> and T<\/jats:styled-content>aenia crassiceps<\/jats:italic> infections, M<\/jats:styled-content>s4a8a expression was detected in hepatic and peritoneal macrophages respectively. Innate immunity in these infections is modulated by T<\/jats:styled-content>oll\u2010like receptor (TLR<\/jats:styled-content>) signaling and TLR<\/jats:styled-content>2\/4\/7 agonists strongly induced M<\/jats:styled-content>s4a8a expression in bone marrow derived macrophages (BMDM<\/jats:styled-content>s) treated with M<\/jats:styled-content>2 mediators (glucocorticoids\/IL<\/jats:styled-content>\u20104). LPS<\/jats:styled-content>\/dexamethasone\/IL<\/jats:styled-content>\u20104\u2010induced M<\/jats:styled-content>s4a8a+<\/jats:sup> BMDM<\/jats:styled-content>s were characterized by strong expression of mRNA<\/jats:styled-content> of mannose receptor<\/jats:italic> (M<\/jats:styled-content>mr<\/jats:italic>), arginase 1,<\/jats:italic> and CD<\/jats:styled-content>163,<\/jats:italic> and by decreased iNOS<\/jats:styled-content><\/jats:italic> expression. Coinduction of M<\/jats:styled-content>s4a8a by M<\/jats:styled-content>2 mediators and TLR<\/jats:styled-content> agonists involved the classical TLR<\/jats:styled-content> signaling cascade via activation of M<\/jats:styled-content>yD<\/jats:styled-content>88\/TRIF<\/jats:styled-content> and NF<\/jats:styled-content>\u2010\u03baB<\/jats:styled-content>. Forced overexpression of M<\/jats:styled-content>s4a8a modulated the TLR<\/jats:styled-content>4 response of RAW<\/jats:styled-content>264.7 cells as shown by gene expression profiling. Upregulation of Hdc, Tcfec,<\/jats:italic> and Sla<\/jats:italic> was confirmed both in primary LPS<\/jats:styled-content>\/dexamethasone\/IL<\/jats:styled-content>\u20104\u2010stimulated M<\/jats:styled-content>s4a8a+<\/jats:sup> BMDM<\/jats:styled-content>s and in peritoneal macrophages from late\u2010stage T<\/jats:styled-content>aenia crassiceps<\/jats:italic> infection. In conclusion, we show that TLR<\/jats:styled-content> signaling skews the typical alternative macrophage activation program to induce a special M<\/jats:styled-content>2\u2010like macrophage subset in vitro that also occurs in immunomodulatory immune reactions in vivo, a process directly involving the CD<\/jats:styled-content>20 homolog M<\/jats:styled-content>s4a8a.<\/jats:p>","DOI":"10.1002\/eji.201142331","type":"journal-article","created":{"date-parts":[[2012,7,19]],"date-time":"2012-07-19T04:56:02Z","timestamp":1342673762000},"page":"2971-2982","source":"Crossref","is-referenced-by-count":14,"title":["The CD<\/scp>20 homolog M<\/scp>s4a8a integrates pro\u2010 and anti\u2010inflammatory signals in novel M<\/scp>2\u2010like macrophages and is expressed in parasite infection"],"prefix":"10.1002","volume":"42","author":[{"given":"Astrid","family":"Schmieder","sequence":"first","affiliation":[{"name":"Department of Dermatology Venereology and Allergology University Medical Center and 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Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yannick","family":"Morias","sequence":"additional","affiliation":[{"name":"Myeloid Cell Immunology Laboratory VIB Brussels Belgium"},{"name":"Cellular and Molecular Immunology Unit Vrije Universiteit Brussel Brussels Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tom","family":"Bosschaerts","sequence":"additional","affiliation":[{"name":"Myeloid Cell Immunology Laboratory VIB Brussels Belgium"},{"name":"Cellular and Molecular Immunology Unit Vrije Universiteit Brussel Brussels Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jan","family":"Van den Bossche","sequence":"additional","affiliation":[{"name":"Myeloid Cell Immunology Laboratory VIB Brussels Belgium"},{"name":"Cellular and Molecular Immunology Unit Vrije Universiteit Brussel Brussels 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