The tumor microenvironment (TME), which is mostly composed of tumor cells, immune cells, signaling molecules, stromal tissue, and the vascular system, is an integrated system that is conducive to the formation of tumors. TME heterogeneity makes the response to immunotherapy different in different tumors, such as "immune-cold" and "immune-hot" tumors. Tumor-associated macrophages, myeloid-derived suppressor cells, and regulatory T cells are the major suppressive immune cells and their different phenotypes interact and influence cancer cells by secreting different signaling factors, thus playing a key role in the formation of the TME as well as in the initiation, growth, and metastasis of cancer cells. Nanotechnology development has facilitated overcoming the obstacles that limit the further development of conventional immunotherapy, such as toxic side effects and lack of targeting. In this review, we focus on the role of three major suppressive immune cells in the TME as well as in tumor development, clinical trials of different drugs targeting immune cells, and different attempts to combine drugs with nanomaterials. The aim is to reveal the relationship between immunotherapy, immunosuppressive TME and nanomedicine, thus laying the foundation for further development of immunotherapy.
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http://dx.doi.org/10.1016/j.biomaterials.2023.122463 | DOI Listing |
Hepatol Commun
November 2024
Human Immunology Laboratory, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, New South Wales, Australia.
Background: HCC develops in the context of chronic inflammation; however, the opposing roles the immune system plays in both the development and control of tumors are not fully understood. Mapping immune cell interactions across the distinct tissue regions could provide greater insight into the role individual immune populations have within tumors.
Methods: A 39-parameter imaging mass cytometry panel was optimized with markers targeting immune cells, stromal cells, endothelial cells, hepatocytes, and tumor cells.
Appl Biochem Biotechnol
January 2025
Computational Biology Lab, Department of Genetic Engineering, School of Bioengineering, SRM Institute of Science and Technology, SRM Nagar, Kattankulathur, 603203, Tamil Nadu, India.
JAK1, a key regulator of multiple oncogenic pathways, is a sought-out target, and its expression in immune cells and tumour-infiltrating lymphocytes (TILs) is associated with a favorable prognosis in breast cancer. JAK1 activates IL-6 via ERBB2 receptor tyrosine kinase signalling and promotes metastatic cancer and STAT3 activation in breast cancer cells. Hence, targeting JAK1 in breast cancer is being explored as a potential therapeutic strategy.
View Article and Find Full Text PDFBull Exp Biol Med
January 2025
Avtsyn Research Institute of Human Morphology, Petrovsky National Research Center of Surgery, Moscow, Russia.
It was previously found that the severity of LPS-induced systemic inflammatory response (SIRS) in rats is determined by resistance to hypoxia and the level of Hif1a expression. Individual differences in the level of Hif1a and NFkb expression in the liver were studied in relation to the severity of inflammatory and immune reactions in LPS-induced SIRS in rats without previous placement in a ventilated decompression chamber. During the early periods after SIRS modeling, rats with high expression of the Hif1a and NFkb genes associated with increased expression of pro- and anti-inflammatory cytokines are identified.
View Article and Find Full Text PDFBackground: Gastric cancer (GC) has a poor prognosis, considerable cellular heterogeneity, and ranks fifth among malignant tumours. Understanding the tumour microenvironment (TME) and intra-tumor heterogeneity (ITH) may lead to the development of novel GC treatments.
Methods: The single-cell RNA sequencing (scRNA-seq) dataset was obtained from the Gene Expression Omnibus (GEO) database, where diverse immune cells were isolated and re-annotated based on cell markers established in the original study to ascertain their individual characteristics.
Arch Dermatol Res
January 2025
Department of Anesthesiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Background: Although the precise cause of the co-occurrence of pyoderma gangrenosum (PG) and inflammatory bowel disease (IBD) is still unknown, prior research has shown that the two conditions coexist. Moreover, it is currently unknown how immune cells function in influencing the relationship between IBD and PG.
Methods: In order to choose independent single nucleotide polymorphism (SNP) as instrumental variables, we were provided with genome-wide association study (GWAS) summary data of European populations from the IEU OpenGWAS project (for IBD) and a the FinnGen database (for PG) publically available.
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