Immune checkpoints (ICPs) are major co-signaling pathways that trigger effector functions in immune cells, with isoforms that are either membrane bound, engaging in direct cell to cell activation locally, or soluble, acting at distant sites by circulating freely or potentially via extracellular vesicles (EVs). Exosomes are small EVs secreted by a variety of cells carrying various proteins and nucleic acids. They are distributed extensively through biological fluids and have major impacts on infectious diseases, cancer, and neuroinflammation. Similarly, ICPs play key roles in a variety of disease conditions and have been extensively utilized as a prognostic tool for various cancers. Herein, we explored if the association between exosomes and ICPs could be a significant contributor of inflammation, particularly in the setting of cancer, neuroinflammation and viral infections, wherein the up regulation in both exosomal proteins and ICPs correlate with immunosuppressive effects. The detailed literature review of existing data highlights the significance and complexity of these two important pathways in mediating cancer and potentiating neuroinflammation via modulating overall immune response.
Can Soluble Immune Checkpoint Molecules on Exosomes Mediate Inflammation?
Creators
Julie Joseph - Drexel University
Benjamin Rahmani - Drexel University
Yonesha Cole - Drexel University
Neha Puttagunta - Drexel University
Edward Lin - Drexel University
Zafar K. Khan - Drexel University
Pooja Jain - Drexel University
Publication Details
Journal of neuroimmune pharmacology
Publisher
Springer Nature
Number of pages
17
Grant note
R01 NS097147 / NIH/NINDS; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Neurological Disorders & Stroke (NINDS)
Resource Type
Journal article
Language
English
Academic Unit
Psychiatry; Microbiology and Immunology; College of Medicine
Web of Science ID
WOS:000710828400002
Scopus ID
2-s2.0-85117888811
Other Identifier
991019167128904721
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