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Title :The CC chemokine ligand (CCL) 1, upregulated by the viral transactivator Tax, can be downregulated by minocycline : possible implications for long-term treatment of HTLV-1-associated myelopathy/tropical spastic paraparesis
Authors :Saito, Mineki
Sejima, Hiroe
Naito, Tadasuke
Ushirogawa, Hiroshi
Matsuzaki, Toshio
Matsuura, Eiji
Tanaka, Yuetsu
Nakamura, Tatsufumi
Takashima, Hiroshi
Issue Date :4-Dec-2017
Abstract :Background:Chemokine (C-C motif) ligand 1 (CCL1) is produced by activated monocytes/ macrophages and T-lymphocytes, and acts as a potent attractant for Th2 cells and a subset of T-regulatory (Treg) cells. Previous reports have indicated that CCL1 is overexpressed in adult T-cell leukemia cells, mediating an autocrine anti-apoptotic loop. Because CCL1 is also known as a potent chemoattractant that plays a major role in inflammatory processes, we investigated the role of CCL1 in the pathogenesis of human T-cell leukemia virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Results:The results showed that: (1) CCL1 was preferentially expressed in HAM/TSP-derived HTLV-1-infected T-cell lines, (2) CCL1 expression was induced along with Tax expression in the Tax-inducible T-cell line JPX9, (3) transient Tax expression in an HTLV-1-negative T-cell line activated the CCL1 gene promoter, (4) plasma levels of CCL1 were significantly higher in patients with HAM/TSP than in HTLV-1-seronegative patients with multiple sclerosis and HTLV-1-infected asymptomatic healthy carriers, and (5) minocycline inhibited the production of CCL1 in HTLV-1-infected T-cell lines. Conclusions:The present results suggest that elevated CCL1 levels may be associated with the pathogenesis of HAM/TSP. Although further studies are required to determine the in vivo significance, minocycline may be considered as a potential candidate for the long-term treatment of HAM/TSP via its anti-inflammatory effects, which includes the inhibition of CCL1 expression.
URL :https://doi.org/10.1186/s12985-017-0902-6
Type Local :雑誌掲載論文
ISSN :1743-422X
Publisher :BioMed Central
URI :http://hdl.handle.net/20.500.12000/46046
Citation :Virology Journal Vol.14
Appears in Collections:Peer-reviewed Journal Articles (Faculty of Medicine)

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