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However, DCs themselves make significant amounts of TSLP in response to microbial products, but little is known about the key downstream signals that induce and modulate this TSLP secretion from human DCs. We show that human monocyte derived DC (mDC) secretion of TSLP in response to <jats:italic>Candida albicans<\/jats:italic> and \u03b2\u2010glucans requires dectin\u20101, Syk, NF\u2010\u03baB, and p38 MAPK signaling. In addition, TSLP production by mDCs is greatly enhanced by IL\u20101\u03b2, but not TNF\u2010\u03b1, in contrast to epithelial cells. Furthermore, TSLP secretion is significantly increased by signals emanating from the endoplasmic reticulum (ER) stress response, specifically the unfolded protein response sensors, inositol\u2010requiring transmembrane kinase\/endonuclease 1 and protein kinase R\u2010like ER kinase, which are activated by dectin\u20101 stimulation. Thus, TSLP production by mDCs requires the integration of signals from dectin\u20101, the IL\u20101 receptor, and ER stress signaling pathways. Autocrine TSLP production is likely to play a role in mDC\u2010controlled immune responses at sites removed from epithelial cell production of the cytokine, such as lymphoid tissue.<\/jats:p>","DOI":"10.1002\/eji.201545537","type":"journal-article","created":{"date-parts":[[2015,11,17]],"date-time":"2015-11-17T07:32:51Z","timestamp":1447745571000},"page":"455-463","source":"Crossref","is-referenced-by-count":44,"title":["TSLP production by dendritic cells is modulated by IL\u20101\u03b2 and components of the endoplasmic reticulum stress response"],"prefix":"10.1002","volume":"46","author":[{"given":"Matthew J.","family":"Elder","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Cambridge School of Clinical Medicine Addenbrookes Hospital  Cambridge UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven J.","family":"Webster","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Cambridge School of Clinical Medicine Addenbrookes Hospital  Cambridge UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David L.","family":"Williams","sequence":"additional","affiliation":[{"name":"Department of Surgery, Center for Inflammation, Infectious Disease and Immunity, James H. 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