Background: While tumor necrosis factor alpha (TNF-�±) inhibitors (TNFi) and other biologics are very effective\nagainst autoimmune diseases, they can also cause infectious diseases. Therefore, it is important to clarify whether\nthe TNFi sometimes used to treat patients with rheumatoid arthritis (RA) complicated with human T-lymphotropic\nvirus type-I (HTLV-I) infection have the unintended side effect of promoting HTLV-I proliferation.\nMethods: We used the HTLV-I-infected cell line HCT-5, derived from spinal fluid cells of a patient with HTLV-I\nassociated myelopathy, to evaluate the production of cytokines and chemokines, TNF-�± receptor (TNFR), the\nexpression of HTLV-I associated genes, the HTLV-I proviral load (PVL), the expression of HTLV-I structural protein,\nand apoptosis. We used Jurkat cells as a control.\nResults: Supernatants of HCT-5 showed time-dependent elevations of IL-6, RANTES and ICAM-1. HCT-5\nsupernatants treated with infliximab, adalimumab, etanercept (ETN), golimumab and certolizumab pegol showed\nno significant differences in the levels of these molecules compared to the control. Neither TNFR1 nor TNFR2\nexpression was altered by any TNFi treatment, relative to phosphate-buffered saline (PBS) treatment, with the\nexception that TNFR2 was significantly decreased and internalized in HCT-5 cells by ETN treatment. The HTLV-I\nassociated genes Tax and HBZ and the PVL levels were not significantly changed. Immunofluorescence staining\nof HCT-5 for an HTLV-I-associated protein, GAG, was also not significantly different between any of the TNFi\ntreatments and the PBS treatment. DNA ladders as an index of apoptosis were not detected. Apoptotic cells were\nnot increased by the addition of any TNFi.\nConclusions: In vitro, TNFi did not affect the cytokine profiles, expression of associated genes and proteins, proviral\nload or apoptosis of HCT-5 cells. The results suggested that TNFi treatment of RA patients complicated with HTLV-I\nmight have no effect on HTLV-I infection.
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