{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T05:29:24Z","timestamp":1791091764270,"version":"4.1.0"},"reference-count":59,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2007,11,22]],"date-time":"2007-11-22T00:00:00Z","timestamp":1195689600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2007,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Mice deficient for the TLR adaptor molecule MyD88 succumb to a local infection with <jats:italic>Leishmania (L.) major<\/jats:italic>. However, the TLR(s) that contribute to the control of this intracellular parasite remain to be defined. Here, we show that TLR9 was required for the induction of IL\u201012 in bone marrow\u2010derived DC by intact <jats:italic>L. major<\/jats:italic> parasites or <jats:italic>L. major<\/jats:italic> DNA and for the early IFN\u2010\u03b3 expression and cytotoxicity of NK cells following infection with <jats:italic>L. major in vivo<\/jats:italic>. During the acute phase of infection TLR9<jats:sup>\u2013\/\u2013<\/jats:sup> mice exhibited more severe skin lesions and higher parasite burdens than C57BL\/6 wild\u2010type controls. Although TLR9 deficiency led to a transient increase of IL\u20104, IL\u201013 and arginase 1 mRNA and a reduced expression of iNOS at the site of infection and in the draining lymph nodes, it did not prevent the development of Th1 cells and the ultimate resolution of the infection. We conclude that TLR9 signaling is essential for NK cell activation, but dispensable for a protective T cell response to <jats:italic>L. major<\/jats:italic> <jats:italic>in vivo<\/jats:italic>.<\/jats:p>","DOI":"10.1002\/eji.200737182","type":"journal-article","created":{"date-parts":[[2007,11,22]],"date-time":"2007-11-22T13:46:36Z","timestamp":1195739196000},"page":"3424-3434","source":"Crossref","is-referenced-by-count":120,"title":["TLR9 signaling is essential for the innate NK cell response in murine cutaneous leishmaniasis"],"prefix":"10.1002","volume":"37","author":[{"given":"Jan","family":"Liese","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulrike","family":"Schleicher","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christian","family":"Bogdan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2007,11,29]]},"reference":[{"key":"e_1_2_8_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0171-2985(11)80366-9"},{"key":"e_1_2_8_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0020-7519(97)00169-0"},{"key":"e_1_2_8_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0065-2776(08)60912-8"},{"key":"e_1_2_8_4_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.166.6.4012"},{"key":"e_1_2_8_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri933"},{"key":"e_1_2_8_6_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.180.3.783"},{"key":"e_1_2_8_7_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.179.4.1367"},{"key":"e_1_2_8_8_2","doi-asserted-by":"crossref","first-page":"4378","DOI":"10.1128\/iai.65.11.4378-4383.1997","article-title":"Interleukin\u201012 is indispensable for protective immunity against Leishmania major.","volume":"65","author":"Mattner F.","year":"1997","journal-title":"Infect. 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