AI Article Synopsis
- Gliomas are the most common and aggressive brain tumors, with glioblastoma patients experiencing a low median survival of only 14 months despite current treatments.
- This study analyzed the role of the immune checkpoint BTN3A1 in 34 Moroccan glioma patients, confirming findings in a larger database and focusing on its expression in glioblastoma.
- High BTN3A1 expression was linked to poorer patient prognosis and a more immunosuppressive environment, indicating that targeting BTN3A1 could be a promising new treatment strategy for advanced gliomas.
Article Abstract
Introduction: Gliomas represent the most prevalent and aggressive tumors within the central nervous system. Despite the current standard treatments, the median survival time for glioblastoma patients remains dismal, hovering around 14 months. While attempts have been made to inhibit the PD-1/PD-L1 and CTLA-4/CD80-CD86 axes through immunotherapy, the outcomes have yet to demonstrate significant efficacy. The immune checkpoint Butyrophilin 3A1 (BTN3A1) can either be involved in advantageous or detrimental function depending on the cancer type.
Methods: In our study, we utilized a Moroccan cohort to delve into the role of BTN3A1 in gliomas. A transcriptomic analysis was conducted on 34 patients, which was then corroborated through a protein analysis in 27 patients and validated using the TCGA database (n = 667).
Results: Our results revealed an elevated expression of BTN3A1 in glioblastoma (grade 4), as evidenced in both the TCGA database and our cohort of Moroccan glioma patients. Within the TCGA cohort, BTN3A1 expression was notably higher in patients with wild-type IDH. We observed a positive correlation between BTN3A1 expression and immune infiltration of B cells, CD8+ T cells, naive CD4+ T cells, and M2 macrophages. Patients exhibiting increased BTN3A1 expression also presented elevated levels of TGF-β, IL-10, and TIM-3 compared to those with reduced BTN3A1 expression. Notably, patients with high BTN3A1 expression were associated with a poorer prognosis than their counterparts with lower expression.
Conclussion: Our findings suggest that BTN3A1 might promote the establishment of an immunosuppressive microenvironment. Consequently, targeting BTN3A1 could offer novel therapeutic avenues for the management of advanced gliomas.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11165028 | PMC |
| http://dx.doi.org/10.3389/fimmu.2024.1397486 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Epstein-Barr Virus BRRF1 Induces Butyrophilin 2A1 in Nasopharyngeal Carcinoma NPC43 Cells via the IL-22/JAK3-STAT3 Pathway.
Int J Mol Sci
December 2024
Department of Biology, Faculty of Science, Hong Kong Baptist University, Kowloon Tong, Hong Kong SAR, China.
Epstein-Barr virus is highly associated with nasopharyngeal carcinoma (NPC) with genes expressed for tumor transformation or maintenance of viral latency, but there are certain genes that can modulate immune molecules. Butyrophilin 2A1 (BTN2A1) is an important activating protein for presenting phosphoantigens for recognition by Vγ9Vδ2 T cells to achieve antitumor activities. We have previously shown that Vγ9Vδ2 T cells achieve efficacy against NPC when BTN2A1 and BTN3A1 are upregulated by stimulating EBV gene expression, particularly LMP1.
View Article and Find Full Text PDFA regulatory variant rs9379874 in T1D risk region 6p22.2 affects BTN3A1 expression regulating T cell function.
Acta Diabetol
October 2024
Department of Endocrinology and Metabolism, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Article Synopsis
- The study focuses on the 6p22.2 genetic region, which is linked to type 1 diabetes (T1D) risk in the Chinese Han population, aiming to explore its associations with T1D subgroups and clinical features.
- A total of 2,608 T1D patients and 4,814 healthy controls from different regions of China were analyzed, identifying the rs4320356 variant as a key player, although it did not relate to islet function or autoimmunity.
- The research revealed that the variant rs9379874 may be the most relevant causal variant for T1D, as it enhances the expression of the BTN3A1 gene and is potentially involved in mechanisms related to T-cell activation
BTN3A1 expressed in cervical cancer cells promotes Vγ9Vδ2 T cells exhaustion through upregulating transcription factors NR4A2/3 downstream of TCR signaling.
Cell Commun Signal
September 2024
Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Article Synopsis
- The study investigates why Vδ2 T cell-based immunotherapy for cervical cancer is not as effective as hoped, focusing on the mechanisms of T cell exhaustion.
- Researchers analyzed tumor samples and cell lines to identify the role of BTN3A1 in enhancing exhaustion markers in Vδ2 T cells, which reduces their ability to fight cancer.
- Findings suggest that inhibiting BTN3A1's effects can rejuvenate Vδ2 T cell function, highlighting potential strategies to improve immunotherapy outcomes in cervical cancer patients.
A Ménage à trois: NLRC5, immunity, and metabolism.
Front Immunol
July 2024
Università della Svizzera Italiana (USI), Faculty of Biomedical Sciences, Institute for Research in Biomedicine, Bellinzona, Switzerland.
The nucleotide-binding and oligomerization domain-like receptors (NLRs) NLR family CARD domain-containing protein 5 (NLRC5) and Class II Major Histocompatibility Complex Transactivator (CIITA) are transcriptional regulators of major histocompatibility complex (MHC) class I and class II genes, respectively. MHC molecules are central players in our immune system, allowing the detection of hazardous 'non-self' antigens and, thus, the recognition and elimination of infected or transformed cells from the organism. Recently, CIITA and NLRC5 have emerged as regulators of selected genes of the butyrophilin () family that interestingly are located in the extended MHC locus.
View Article and Find Full Text PDFIdentification of drug targets for Sjögren's syndrome: multi-omics Mendelian randomization and colocalization analyses.
Front Immunol
June 2024
Department of Stomatology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
Background: Targeted therapy for Sjögren's syndrome (SS) has become an important focus for clinicians. Multi-omics-wide Mendelian randomization (MR) analyses have provided new ideas for identifying potential drug targets.
Methods: We conducted summary-data-based Mendelian randomization (SMR) analysis to evaluate therapeutic targets associated with SS by integrating DNA methylation, gene expression and protein quantitative trait loci (mQTL, eQTL, and pQTL, respectively).
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!