@article{PAR00011482,
  title = {{T}he {C}-type lectin receptors dectin-1, {MR}, and {SIGNR}3 contribute both positively and negatively to the macrophage response to {L}eishmania infantum},
  author = {{L}efevre, {L}. and {L}ugo-{V}illarino, {G}. and {M}eunier, {E}. and {V}alentin, {A}. and {O}lagnier, {D}. and {A}uthier, {H}. and {D}uval, {C}. and {D}ardenne, {C}. and {B}ernad, {J}. and {L}emesre, {J}ean-{L}oup and {A}uwerx, {J}. and {N}eyrolles, {O}. and {P}ipy, {B}. and {C}oste, {A}.},
  editor = {},
  language = {{ENG}},
  abstract = {{M}acrophages act as the primary effector cells during {L}eishmania infection through production of reactive oxygen species ({ROS}) and interleukin-1 beta ({IL}-1 beta). {H}owever, how macrophage-killing mechanisms are activated during {L}eishmania-macrophage interactions is poorly understood. {H}ere, we report that the macrophage response against {L}eishmania infantum in vivo is characterized by an {M}2b-like phenotype and {C}-type lectin receptors ({CLR}s) signature composed of {D}ectin-1, mannose receptor ({MR}), and the {DC}-{SIGN} homolog {SIGNR}3 expression. {D}ectin-1 and {MR} were crucial for the microbicidal response as indicated by the fact that they activated {S}yk-p47phox and arachidonic acid ({AA})-{NADPH} oxidase signaling pathways, respectively, needed for {ROS} production and also triggered {S}yk-coupled signaling for caspase-1-induced {IL}-1 beta secretion. {I}n contrast, {SIGNR}3 has divergent functions during {L}eishmania infantum pathogenesis; this {CLR} favored parasite resilience through inhibition of the {LTB}4-{IL}-1 beta axis. {T}hese pathways also operated during infection of primary human macrophages. {T}herefore, our study promotes {CLR}s as potential targets for treatment, diagnosis, and prevention of visceral leishmaniasis.},
  keywords = {},
  booktitle = {},
  journal = {{I}mmunity},
  volume = {38},
  numero = {5},
  pages = {1038--1049},
  ISSN = {1074-7613},
  year = {2013},
  DOI = {10.1016/j.immuni.2013.04.010},
  URL = {https://www.documentation.ird.fr/hor/{PAR}00011482},
}