CD86 x OX40L x CD80

Last update 08 May 2025

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CD86OX40LCD80

100 Clinical Results associated with CD86 x OX40L x CD80

100 Translational Medicine associated with CD86 x OX40L x CD80

0 Patents (Medical) associated with CD86 x OX40L x CD80

Literatures (Medical) associated with CD86 x OX40L x CD80

12 Feb 2025·Recent Patents on Anti-Cancer Drug Discovery

Bioinformatics Analysis of Key Genes Associated with Resistance to the Combination of Bevacizumab and Pemetrexed Chemotherapy in Non-small Cell Lung Cancer

Article

Author: Sun, Qian ; Hu, Chenling ; Chen, Siwen ; Pan, Xudong ; Xu, Shenjie

Objective:This study aimed to identify key genes linked to resistance to a combination treatment regimen of bevacizumab and pemetrexed in non-small cell lung cancer (NSCLC) through bioinformatics analysis and analysis of their associated pathways.Methods:Expression data from the Gene Expression Omnibus (GEO) database (GSE154286) were analyzed. The differentially expressed genes (DEGs) between tissues sensitive and resistant to combined bevacizumab and pemetrexed treatment in NSCLC were identified. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment was investigated, and protein-protein interaction (PPI) networks, as well as transcription factor (TFs)- DEGs-miRNA networks, were created using the STRING tool. Key genes were identified with the help of the MCODE plugin. Additionally, gene set enrichment analysis (GSEA) was utilized to identify pathways linked to the key genes. A retrospective analysis was conducted on clinical data from 80 NSCLC patients. Patients were categorized into drug-resistant and non-resistant groups based on RECIST1.1 criteria. The expression of the key gene TNFSF4 was analyzed using quantitative real-time PCR (qRT-PCR).Results:In the GSE154286 dataset, 35 downregulated DEGs were discovered. KEGG pathway enrichment analysis revealed that these DEGs were primarily associated with immunity and inflammation-related pathways. The PPI network construction highlighted a significant module and led to the identification of 8 candidate genes: TNFRSF18, TNFSF4, LGALS9, FAS, LAG3, CD86, CD80, and FOXP3. The TFs-DEGs-miRNA network analysis pinpointed TNFSF4 as a key gene, potentially regulated by 7 transcription factors and interacting with 9 miRNAs. GSEA analysis suggested that TNFSF4 may influence NSCLC’s pathological processes through involvement in pathways involved in chemokine, JAK/STAT, NOD-like receptor, T cell receptor, toll-like receptor, and PPAR signaling. qRT-PCR detection displayed significantly lower expression of TNFSF4 in the peripheral blood of the patients in the resistant group relative to the non-resistant group (p < 0.0001). Logistic regression analysis showed that low TNFSF4 levels were independently linked to a raised risk of resistance to bevacizumab combined with pemetrexed therapy in lung adenocarcinoma patients.Conclusion:The identification of key genes, such as TNFSF4, and resistance-related signaling pathways through bioinformatics analysis offers valuable insights into potential mechanisms of chemotherapy resistance in NSCLC when treated with the combination of bevacizumab and pemetrexed. These findings provide a theoretical foundation for advancing clinical research on diagnosis and treatment.

01 Oct 2023·European Journal of Immunology

Skin‐derived TSLP stimulates skin migratory dendritic cells to promote the expansion of regulatory T cells

Article

Author: Yokoyama, Yuichi ; Kambayashi, Taku ; Tanaka, Yukinori

AbstractTherapeutic strategies that enhance regulatory T (Treg) cell proliferation or suppressive function hold promise for the treatment of autoimmune and inflammatory diseases. We previously reported that the topical application of the vitamin D3 analog MC903 systemically expands Treg cells by stimulating the production of thymic stromal lymphopoietin (TSLP) from the skin. Using mice lacking TSLP receptor expression by dendritic cells (DCs), we hereby show that TSLP receptor signaling in DCs is required for this Treg expansion in vivo. Topical MC903 treatment of ear skin selectively increased the number of migratory DCs in skin‐draining lymph nodes (LNs) and upregulated their expression of co‐stimulatory molecules. Accordingly, DCs isolated from skin‐draining LNs but not mesenteric LNs or spleen of MC903‐treated mice showed an enhanced ability to promote Treg proliferation, which was driven by co‐stimulatory signals through CD80/CD86 and OX40 ligand. Among the DC subsets in the skin‐draining LNs of MC903‐treated mice, migratory XCR1−CD11b+ type 2 and XCR1−CD11b− double negative conventional DCs promoted Treg expansion. Together, these data demonstrate that vitamin D3 stimulation of skin induces TSLP expression, which stimulates skin migratory DCs to expand Treg cells. Thus, topical MC903 treatment could represent a convenient strategy to treat inflammatory disorders by engaging this pathway.

01 Sep 2023·The Journal of Immunology

TGF-β Signaling Prevents MHC Class II–Expressing Lymphatic Endothelial Cells from Reactivating Human Allogenic Memory CD4+ T Cells

Article

Author: Salles, Calixto M ; Potin, Lambert ; Swartz, Melody A ; Gomez Medellin, J Emiliano ; Mezyk-Kopec, Renata

AbstractLymphatic endothelial cells (LECs) express MHC class II (MHC-II) upon IFN-γ stimulation, yet recent evidence suggests that LECs cannot activate naive or memory CD4+ T cells. In this article, we show that IFN-γ–activated human dermal LECs can robustly reactivate allogeneic human memory CD4+ T cells (hCD4+ TMs), but only when TGF-β signaling is inhibited. We found that in addition to upregulating MHC-II, IFN-γ also induces LECs to upregulate glycoprotein A repetitions predominant, which anchors latent TGF-β to the membrane and potentially inhibits T cell activation. Indeed, hCD4+ TM proliferation was substantially increased when LEC-CD4+ TM cultures were treated with a TGF-β receptor type 1 inhibitor or when glycoprotein A repetitions predominant expression was silenced in LECs. Reactivated hCD4+ TMs were characterized by their proliferation, CD25 expression, and cytokine secretion. CD4+ TM reactivation was dependent on LEC expression of MHC-II, confirming direct TCR engagement. Although CD80 and CD86 were not detected on LECs, the costimulatory molecules OX40L and ICOSL were upregulated upon cytokine stimulation; however, blocking these did not affect CD4+ TM reactivation by LECs. Finally, we found that human dermal LECs also supported the maintenance of Foxp3-expressing hCD4+ TMs independently of IFN-γ–induced MHC-II. Together, these results demonstrate a role for LECs in directly modulating CD4+ TM reactivation under inflammatory conditions and point to LEC-expressed TGF-β as a negative regulator of this activation.

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