{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T20:28:48Z","timestamp":1791404928619,"version":"4.3.3"},"reference-count":40,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2015,1,22]],"date-time":"2015-01-22T00:00:00Z","timestamp":1421884800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Parasite Immunology"],"published-print":{"date-parts":[[2015,2]]},"abstract":"Summary<\/jats:title>Filarial infection in humans is initiated when a mosquito deposits third\u2010stage parasite larvae (L3) in the skin. Langerhans cells (LC<\/jats:styled-content>s) and dermal dendritic cells (DDC<\/jats:styled-content>s) are the first cells that the parasite encounters, and L3s must evade these highly effective antigen\u2010presenting cells to establish infection. To assess LC<\/jats:styled-content> and DDC<\/jats:styled-content> responses to L3 in human skin, we employed three models of increasing physiologic relevance: in vitro<\/jats:italic>\u2010generated LC<\/jats:styled-content>s, epidermal blister explants and full\u2010thickness human skin sections. In vitro\u2010generated LC<\/jats:styled-content>s expressed TLR<\/jats:styled-content>1\u201010 and robustly produced IL<\/jats:styled-content>\u20106 and TNF<\/jats:styled-content>\u2010\u03b1 in response to PolyI:C, but pre\u2010exposure to L3s did not alter inflammatory cytokine production or TLR<\/jats:styled-content> expression. L3s did not modulate expression of LC<\/jats:styled-content> markers CDH<\/jats:styled-content>1, CD<\/jats:styled-content>207, or CD<\/jats:styled-content>1a, or the regulatory products TSLP<\/jats:styled-content> or IDO<\/jats:styled-content> in epidermal explants or in vitro<\/jats:italic>\u2010generated LC<\/jats:styled-content>. LC<\/jats:styled-content>, CD<\/jats:styled-content>14+ DDC<\/jats:styled-content>, CD<\/jats:styled-content>1c+ DC<\/jats:styled-content> and CD<\/jats:styled-content>141+ DC<\/jats:styled-content> from human skin sections were analysed by flow cytometry. While PolyI:C potently induced CCL<\/jats:styled-content>22 production in LC<\/jats:styled-content>, CD<\/jats:styled-content>1c+ DC<\/jats:styled-content>, and CD<\/jats:styled-content>141+ DC<\/jats:styled-content>, and IL<\/jats:styled-content>\u201010 production in LC<\/jats:styled-content>, L3s did not modulate the numbers of or cytokine production by any skin DC<\/jats:styled-content> subset. L3s broadly failed to activate or modulate LC<\/jats:styled-content>s or DDC<\/jats:styled-content>s, suggesting filarial larvae expertly evade APC<\/jats:styled-content> detection in human skin.<\/jats:p>","DOI":"10.1111\/pim.12169","type":"journal-article","created":{"date-parts":[[2014,12,27]],"date-time":"2014-12-27T15:12:44Z","timestamp":1419693164000},"page":"79-91","source":"Crossref","is-referenced-by-count":11,"title":["Brugia malayi<\/i> infective larvae fail to activate Langerhans cells and dermal dendritic cells in human skin"],"prefix":"10.1111","volume":"37","author":[{"given":"R. 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