{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T10:30:29Z","timestamp":1790937029655,"version":"4.1.0"},"reference-count":34,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2004,4,1]],"date-time":"2004-04-01T00:00:00Z","timestamp":1080777600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2004,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>The control of<jats:italic>Listeria monocytogenes<\/jats:italic>infection depends on the rapid activation of the innate immune system, likely through Toll-like receptors (TLR), since mice deficient for the common adapter protein of TLR signaling, myeloid differentiation factor 88 (MyD88), succumb to<jats:italic>Listeria<\/jats:italic>infection. In order to test whether TLR2 is involved in the control of infections, we compared the host response in TLR2-deficient mice with that in wild-type mice. Here we show that TLR2-deficient mice are more susceptible to systemic infection by<jats:italic>Listeria<\/jats:italic>than are wild-type mice, with a reduced survival rate, increased bacterial burden in the liver, and abundant and larger hepatic microabscesses containing increased numbers of neutrophils. The production of tumor necrosis factor, interleukin-12, and nitric oxide and the expression of the costimulatory molecules CD40 and CD86, which are necessary for the control of infection, were reduced in TLR2-deficient macrophages and dendritic cells stimulated by<jats:italic>Listeria<\/jats:italic>and were almost abolished in the absence of MyD88, coincident with the high susceptibility of MyD88-deficient mice to in vivo infection. Therefore, the present data demonstrate a role for TLR2 in the control of<jats:italic>Listeria<\/jats:italic>infection, but other MyD88-dependent signals may contribute to host resistance.<\/jats:p>","DOI":"10.1128\/iai.72.4.2131-2139.2004","type":"journal-article","created":{"date-parts":[[2004,3,23]],"date-time":"2004-03-23T22:43:10Z","timestamp":1080081790000},"page":"2131-2139","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":148,"title":["Toll-Like Receptor 2 Is Required for Optimal Control of<i>Listeria monocytogenes<\/i>Infection"],"prefix":"10.1128","volume":"72","author":[{"given":"David","family":"Torres","sequence":"first","affiliation":[{"name":"CNRS, Laboratoire de Ge\u0301ne\u0301tique expe\u0301rimentale et mole\u0301culaire (GEM2358), F-45071 Orle\u0301ans Cedex 2, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mathieu","family":"Barrier","sequence":"additional","affiliation":[{"name":"CNRS, Laboratoire de Ge\u0301ne\u0301tique expe\u0301rimentale et mole\u0301culaire (GEM2358), F-45071 Orle\u0301ans Cedex 2, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Franck","family":"Bihl","sequence":"additional","affiliation":[{"name":"CNRS, Laboratoire de Ge\u0301ne\u0301tique expe\u0301rimentale et mole\u0301culaire (GEM2358), F-45071 Orle\u0301ans Cedex 2, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Valerie J. 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