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An epigenetic pathway regulates MHC-II expression and function in B cell lymphoma models.
J Clin Invest
January 2025
Department of Biochemistry and Molecular Genetics and.
Mutations or homozygous deletions of MHC class II (MHC-II) genes are commonly found in B cell lymphomas that develop in immune-privileged sites and have been associated with patient survival. However, the mechanisms regulating MHC-II expression, particularly through genetic and epigenetic factors, are not yet fully understood. In this study, we identified a key signaling pathway involving the histone H2AK119 deubiquitinase BRCA1 associated protein 1 (BAP1), the interferon regulatory factor interferon regulatory factor 1 (IRF1), and the MHC-II transactivator class II transactivator (CIITA), which directly activates MHC-II gene expression.
View Article and Find Full Text PDFCirsii Herba glycoprotein promotes macrophage M1 polarization through MAPK and NF-κB signaling pathways via interaction with TLR4.
Int J Biol Macromol
January 2025
MOA Key Laboratory of Animal Virology, Center for Veterinary Sciences, Department of Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China. Electronic address:
The present study aimed to extract and purify the glycoprotein from Cirsii Herba (CHPs), and investigate its immunomodulatory activity and molecular mechanism in RAW264.7 macrophages. The results showed that CHPs contained 14.
View Article and Find Full Text PDFANXA10 sensitizes microsatellite instability-high colorectal cancer to anti-PD-1 immunotherapy via assembly of HLA-DR dimers by regulating CD74.
Cell Biol Toxicol
January 2025
Department of Medical Oncology, the First Hospital of China Medical University, Shenyang, Liaoning, China.
Background: Microsatellite instability-high (MSI-H) metastatic colorectal cancer (CRC) patients are the dominant population in immune checkpoint blockade treatments, while more than half of them could not benefit from single-agent immunotherapy. We tried to identify the biomarker of MSI-H CRC and explore its role and mechanism in anti-PD-1 treatments. Tumor-specific MHC-II was linked to a better response to anti-PD-1 in MSI-H CRC and CD74 promoted assembly and transport of HLA-DR dimers.
View Article and Find Full Text PDFUnlabelled: Regulatory T cells (T cells) play a critical role in suppressing anti-tumor immunity, often resulting in unfavorable clinical outcomes across numerous cancers. However, systemic T depletion, while augmenting anti-tumor responses, also triggers detrimental autoimmune disorders. Thus, dissecting the mechanisms by which T cells navigate and exert their functions within the tumor microenvironment (TME) is pivotal for devising innovative T -centric cancer therapies.
View Article and Find Full Text PDFDefective removal of invariant chain peptides from MHC class II suppresses tumor antigen presentation and promotes tumor growth.
Cell Rep
January 2025
Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address:
Tumor-draining lymph node dendritic cells (DCs) are poor stimulators of tumor antigen-specific CD4 T cells; however, the mechanism behind this defect is unclear. We now show that, in tumor-draining lymph node DCs, a large proportion of major histocompatibility complex class II (MHC-II) molecules retains the class II-associated invariant chain peptide (CLIP) fragment of the invariant chain bound to the MHC-II peptide binding groove due to reduced expression of the peptide editor H2-M and enhanced activity of the CLIP-generating proteinase cathepsin S. The net effect of this is that MHC-II molecules are unable to efficiently bind antigenic peptides.
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