000199137 001__ 199137
000199137 005__ 20181203023513.0
000199137 0247_ $$2doi$$a10.1016/j.immuni.2013.04.010
000199137 022__ $$a1074-7613
000199137 02470 $$2ISI$$a000330942500020
000199137 037__ $$aARTICLE
000199137 245__ $$aThe C-type Lectin Receptors Dectin-1, MR, and SIGNR3 Contribute Both Positively and Negatively to the Macrophage Response to Leishmania infantum
000199137 260__ $$bElsevier$$c2013$$aCambridge
000199137 269__ $$a2013
000199137 300__ $$a12
000199137 336__ $$aJournal Articles
000199137 520__ $$aMacrophages act as the primary effector cells during Leishmania infection through production of reactive oxygen species (ROS) and interleukin-1 beta (IL-1 beta). However, how macrophage-killing mechanisms are activated during Leishmania-macrophage interactions is poorly understood. Here, we report that the macrophage response against Leishmania infantum in vivo is characterized by an M2b-like phenotype and C-type lectin receptors (CLRs) signature composed of Dectin-1, mannose receptor (MR), and the DC-SIGN homolog SIGNR3 expression. Dectin-1 and MR were crucial for the microbicidal response as indicated by the fact that they activated Syk-p47phox and arachidonic acid (AA)-NADPH oxidase signaling pathways, respectively, needed for ROS production and also triggered Syk-coupled signaling for caspase-1-induced IL-1 beta secretion. In contrast, SIGNR3 has divergent functions during Leishmania infantum pathogenesis; this CLR favored parasite resilience through inhibition of the LTB4-IL-1 beta axis. These pathways also operated during infection of primary human macrophages. Therefore, our study promotes CLRs as potential targets for treatment, diagnosis, and prevention of visceral leishmaniasis.
000199137 700__ $$uUniv Toulouse, UPS, UMR PHARMA DEV 152, F-31432 Toulouse, France$$aLefevre, Lise
000199137 700__ $$uUniv Toulouse, UPS, UMR PHARMA DEV 152, F-31432 Toulouse, France$$aLugo-Villarino, Geanncarlo
000199137 700__ $$uUniv Toulouse, UPS, UMR PHARMA DEV 152, F-31432 Toulouse, France$$aMeunier, Etienne
000199137 700__ $$uUniv Toulouse, UPS, UMR PHARMA DEV 152, F-31432 Toulouse, France$$aValentin, Alexis
000199137 700__ $$uUniv Toulouse, UPS, UMR PHARMA DEV 152, F-31432 Toulouse, France$$aOlagnier, David
000199137 700__ $$uUniv Toulouse, UPS, UMR PHARMA DEV 152, F-31432 Toulouse, France$$aAuthier, Helene
000199137 700__ $$uCNRS, IPBS, F-31077 Toulouse, France$$aDuval, Carine
000199137 700__ $$uUniv Toulouse, UPS, UMR PHARMA DEV 152, F-31432 Toulouse, France$$aDardenne, Christophe
000199137 700__ $$uUniv Toulouse, UPS, UMR PHARMA DEV 152, F-31432 Toulouse, France$$aBernad, Jose
000199137 700__ $$uIRD Ctr CIRAD, F-34394 Montpellier, France$$aLemesre, Jean Loup
000199137 700__ $$0240040$$g185233$$aAuwerx, Johan
000199137 700__ $$uCNRS, IPBS, F-31077 Toulouse, France$$aNeyrolles, Olivier
000199137 700__ $$uUniv Toulouse, UPS, UMR PHARMA DEV 152, F-31432 Toulouse, France$$aPipy, Bernard
000199137 700__ $$aCoste, Agnes$$uUniv Toulouse, UPS, UMR PHARMA DEV 152, F-31432 Toulouse, France
000199137 773__ $$j38$$tImmunity$$k5$$q1038-1049
000199137 909C0 $$xU11905$$0252023$$pNCEM
000199137 909CO $$pSV$$particle$$ooai:infoscience.tind.io:199137
000199137 917Z8 $$x196843
000199137 937__ $$aEPFL-ARTICLE-199137
000199137 973__ $$rREVIEWED$$sPUBLISHED$$aOTHER
000199137 980__ $$aARTICLE