Glycan-Lectin Interactions as Novel Immunosuppression Drivers in Glioblastoma.

Int J Mol Sci

Laboratory of Tumor Immunology and Cell Therapy, Department of Experimental Medicine, "Sapienza" University of Rome, Viale Regina Elena 324, 00161 Rome, Italy.

Published: June 2022

AI Article Synopsis

  • Glioblastoma (GB) remains a challenging brain tumor in adults, emphasizing the need for new therapeutic targets due to its aggressive nature.
  • Lectins, which are proteins that bind sugars, play a crucial role in regulating various biological processes and are implicated in GB's progression and immune evasion through alterations in glycosylation.
  • The study highlights the involvement of immune cells and specific immune-related lectin receptors in promoting a suppressive tumor microenvironment, suggesting they could be potential targets for innovative therapies.

Article Abstract

Despite diagnostic and therapeutic improvements, glioblastoma (GB) remains one of the most threatening brain tumor in adults, underlining the urgent need of new therapeutic targets. Lectins are glycan-binding proteins that regulate several biological processes through the recognition of specific sugar motifs. Lectins and their ligands are found on immune cells, endothelial cells and, also, tumor cells, pointing out a strong correlation among immunity, tumor microenvironment and vascularization. In GB, altered glycans and lectins contribute to tumor progression and immune evasion, shaping the tumor-immune landscape promoting immunosuppressive cell subsets, such as myeloid-derived suppressor cells (MDSCs) and M2-macrophages, and affecting immunoeffector populations, such as CD8 T cells and dendritic cells (DCs). Here, we discuss the latest knowledge on the immune cells, immune related lectin receptors (C-type lectins, Siglecs, galectins) and changes in glycosylation that are involved in immunosuppressive mechanisms in GB, highlighting their interest as possible novel therapeutical targets.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9181495PMC
http://dx.doi.org/10.3390/ijms23116312DOI Listing

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