@article{fdi:010071461,
  title = {{LRH}-1 mediates anti-inflammatory and antifungal phenotype of {IL}-13-activated macrophages through the {PPAR} gamma ligand synthesis},
  author = {{L}efevre, {L}. and {A}uthier, {H}. and {S}tein, {S}. and {M}ajorel, {C}larisse and {C}ouderc, {B}. and {D}ardenne, {C}. and {E}ddine, {M}. {A}. and {M}eunier, {E}. and {B}ernad, {J}. and {V}alentin, {A}. and {P}ipy, {B}. and {S}choonjans, {K}. and {C}oste, {A}.},
  editor = {},
  language = {{ENG}},
  abstract = {{L}iver receptor homologue-1 ({LRH}-1) is a nuclear receptor involved in the repression of inflammatory processes in the hepatointestinal tract. {H}ere we report that {LRH}-1 is expressed in macrophages and induced by the {T}h2 cytokine {IL}-13 via a mechanism involving {STAT}6. {W}e show that loss-of-function of {LRH}-1 in macrophages impedes {IL}-13-induced macrophage polarization due to impaired generation of 15-{HETE} {PPAR} gamma ligands. {T}he incapacity to generate 15-{HETE} metabolites is at least partially caused by the compromised regulation of {CYP}1{A}1 and {CYP}1{B}1. {M}ice with {LRH}-1-deficient macrophages are, furthermore, highly susceptible to gastrointestinal and systemic {C}andida albicans infection. {A}ltogether, these results identify {LRH}-1 as a critical component of the anti-inflammatory and fungicidal response of alternatively activated macrophages that acts upstream from the {IL}-13-induced 15-{HETE}/{PPAR} gamma axis.},
  keywords = {},
  booktitle = {},
  journal = {{N}ature {C}ommunications},
  volume = {6},
  numero = {},
  pages = {art. 6801 [13 p.]},
  ISSN = {2041-1723},
  year = {2015},
  DOI = {10.1038/ncomms7801},
  URL = {https://www.documentation.ird.fr/hor/fdi:010071461},
}