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http://purl.uniprot.org/citations/37981615http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/37981615http://www.w3.org/2000/01/rdf-schema#comment"

Background

Triple-negative breast cancers (TNBC) are highly aggressive malignancies with poor prognosis. As an essential enzyme in the tryptophan-kynurenine metabolic pathway, indoleamine 2,3 dioxygenase-1 (IDO-1) has been reported to facilitate immune escape of various tumors. However, the mechanism underlying the immunosuppressive role of IDO-1 in TNBC remains largely uncharacterized.

Methods

We examined the IDO-1 expression in 93 clinical TNBC tissues and paired adjacent normal tissues, and analyzed the regulation role of environmental cytokines like IFN-γ in IDO-1 expression. The effect of IDO-1 expression in TNBC cells on the function of NK cells were then evaluated and the underlying mechanisms were exploited.

Results

IDO-1 expressed in 50 of 93 (54.1%) TNBC patients. TNBC patients with high IDO-1 expression tended to have more infiltrated immune cells including NK cells, which are less active than patients with low IDO-1 expression. NK cells could produce IFN-γ, which induced IDO-1 expression in TNBC cells, whereas IDO-1 impaired the cytotoxicity of co-cultured NK cells by upregulation of HLA-G. Blockade of HLA-G improved the antitumor activity of NK cells to TNBC in vivo.

Conclusion

TNBC cells induce dysfunction of NK cells through an IFN-γ/IDO-1/HLA-G pathway, which provide novel insights into the mechanisms of TNBC progression and demonstrate the applicability of IDO-1 and HLA-G targeting in the treatment of TNBC."xsd:string
http://purl.uniprot.org/citations/37981615http://purl.org/dc/terms/identifier"doi:10.1007/s12282-023-01522-w"xsd:string
http://purl.uniprot.org/citations/37981615http://purl.uniprot.org/core/author"Li W."xsd:string
http://purl.uniprot.org/citations/37981615http://purl.uniprot.org/core/author"Zhang P."xsd:string
http://purl.uniprot.org/citations/37981615http://purl.uniprot.org/core/author"Ren H."xsd:string
http://purl.uniprot.org/citations/37981615http://purl.uniprot.org/core/author"Zheng G."xsd:string
http://purl.uniprot.org/citations/37981615http://purl.uniprot.org/core/author"Jia L."xsd:string
http://purl.uniprot.org/citations/37981615http://purl.uniprot.org/core/author"Bai S."xsd:string
http://purl.uniprot.org/citations/37981615http://purl.uniprot.org/core/author"Jing R."xsd:string
http://purl.uniprot.org/citations/37981615http://purl.uniprot.org/core/date"2024"xsd:gYear
http://purl.uniprot.org/citations/37981615http://purl.uniprot.org/core/name"Breast Cancer"xsd:string
http://purl.uniprot.org/citations/37981615http://purl.uniprot.org/core/pages"135-147"xsd:string
http://purl.uniprot.org/citations/37981615http://purl.uniprot.org/core/title"IDO-1 impairs antitumor immunity of natural killer cells in triple-negative breast cancer via up-regulation of HLA-G."xsd:string
http://purl.uniprot.org/citations/37981615http://purl.uniprot.org/core/volume"31"xsd:string
http://purl.uniprot.org/citations/37981615http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/37981615
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