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UC ‐1V150, a potent TLR 7 agonist capable of activating macrophages and potentiating mA b‐mediated target cell deletion
Author(s) -
Dahal L. N.,
Gadd A.,
Edwards A. D.,
Cragg M. S.,
Beers S. A.
Publication year - 2018
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12666
Subject(s) - tlr7 , immune system , chemokine , innate immune system , cytokine , agonist , immunology , autoimmunity , biology , toll like receptor , receptor , inflammation , tlr9 , acquired immune system , microbiology and biotechnology , cancer research , biochemistry , gene expression , dna methylation , gene
Abstract Toll‐like receptors ( TLR ) are critical mediators of the immune system with their activation linked to infection, inflammation and the pathogenesis of immune diseases including autoimmunity and cancer. For this reason, over the last 2 decades, TLR and their associated signalling pathways have been targeted therapeutically to enhance innate and adaptive immunity. Several TLR ligands, both endogenous and synthetic are at various phases of clinical testing, and new ligands are continually emerging. Agonists of TLR 7 are known immune response modifiers, simultaneously stimulating several cell types, resulting in immune cell activation and cytokine and chemokine release. The immune stimulating properties of the TLR 7 agonist Imiquimod has also been exploited for use in the treatment of malignant superficial tumours of the skin. Here, we investigated a novel TLR 7 agonist UC ‐1V150 and demonstrate it activates both human and mouse myeloid cells in vitro and in vivo, to deliver potent FcγR‐mediated engulfment of opsonized target cells.