HLA-G has been widely implicated in advanced cancers through different pathways of immunosuppression allowing tumor escape. Contrarily, HLA-E has a controversial role in the tumor escape from the immune system. IDO catabolic enzyme is known to be up-regulated in many tumors types allowing their immune escape. Based on these considerations, we investigated the expression of HLA-G, HLA-E and IDO molecules in endometrial cancer (EC) and their association with prognostic clinicopathologic parameters. Their expression were checked in tumoral and adjacent endometrial tissues. Both HLA-G and IDO immunostaining were significantly increased in EC tissues compared to normal residual endometrial glands (Mann Whitney U-test, p = 0.0001 and p = 0,020 respectively). However, HLA-E was highly expressed in tumoral tissues as well as in normal residual endometrial glands (respectively, 100% and 81.8%). Increased HLA-G expression levels were observed in high histological grade (grade 3), and in the non-endometrioid type 2 EC. Unexpectedly, patients with IDO Low expression had significantly impaired overall survival compared to patients with IDO High (log-rank p = 0.021). Conversely, HLA-E low expression was associated to an improved overall survival EC (log-rank p = 0.004). We concluded that, HLA-G and IDO are highly expressed in EC compared to adjacent normal endometrial tissues, that might be interesting for the EC outcome.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.humimm.2020.03.008 | DOI Listing |
Cancers (Basel)
December 2024
Department of Immunology, IML and IdISSC, Hospital Clinico San Carlos, 28040 Madrid, Spain.
Human leukocyte antigens (HLAs) are essential regulators of immune responses against cancer, with classical HLAs well-documented for their role in tumor recognition and immune surveillance. In recent years, non-classical HLAs-including HLA-E, HLA-F, HLA-G, and HLA-H-have emerged as critical players in the immune landscape of cancer due to their diverse and less conventional functions in immune modulation. These molecules exhibit unique mechanisms that enable tumors to escape immune detection, promote tumor progression, and contribute to therapeutic resistance.
View Article and Find Full Text PDFHLA
October 2024
Anthony Nolan Research Institute, Royal Free Hospital, London, UK.
Eight novel HLA class I alleles have been identified using full gene sequencing.
View Article and Find Full Text PDFHum Immunol
November 2024
Centre for Immune Regulation and Reproductive Immunology (CIRRI), Department of Clinical Biochemistry, Zealand University Hospital, Roskilde, Denmark; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Electronic address:
Triple-negative breast cancer (TNBC) is usually aggressive and challenging to treat. With high tumour immunogenicity TNBC patients might benefit from immunotherapy. We evaluated heterogeneous immune profiles of individual tumours in relation to clinical development to identify immune markers and their mutual expression.
View Article and Find Full Text PDFPLoS Comput Biol
September 2024
Finnish Red Cross Blood Service, Research and Development, Helsinki, Finland.
In addition to the classical HLA genes, the major histocompatibility complex (MHC) harbors a high number of other polymorphic genes with less established roles in disease associations and transplantation matching. To facilitate studies of the non-classical and non-HLA genes in large patient and biobank cohorts, we trained imputation models for MICA, MICB, HLA-E, HLA-F and HLA-G alleles on genome SNP array data. We show, using both population-specific and multi-population 1000 Genomes references, that the alleles of these genes can be accurately imputed for screening and research purposes.
View Article and Find Full Text PDFJ Heart Lung Transplant
December 2024
Center of Virology, Medical University Vienna, Vienna, Austria. Electronic address:
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!