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Research Article Free access | 10.1172/JCI116789

Infection of human synovial cells by human T cell lymphotropic virus type I. Proliferation and granulocyte/macrophage colony-stimulating factor production by synovial cells.

M Sakai, K Eguchi, K Terada, M Nakashima, I Yamashita, H Ida, Y Kawabe, T Aoyagi, H Takino, and T Nakamura

First Department of Internal Medicine, Nagasaki University School of Medicine, Japan.

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First Department of Internal Medicine, Nagasaki University School of Medicine, Japan.

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First Department of Internal Medicine, Nagasaki University School of Medicine, Japan.

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First Department of Internal Medicine, Nagasaki University School of Medicine, Japan.

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First Department of Internal Medicine, Nagasaki University School of Medicine, Japan.

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First Department of Internal Medicine, Nagasaki University School of Medicine, Japan.

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First Department of Internal Medicine, Nagasaki University School of Medicine, Japan.

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First Department of Internal Medicine, Nagasaki University School of Medicine, Japan.

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First Department of Internal Medicine, Nagasaki University School of Medicine, Japan.

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First Department of Internal Medicine, Nagasaki University School of Medicine, Japan.

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Published October 1, 1993 - More info

Published in Volume 92, Issue 4 on October 1, 1993
J Clin Invest. 1993;92(4):1957–1966. https://doi.org/10.1172/JCI116789.
© 1993 The American Society for Clinical Investigation
Published October 1, 1993 - Version history
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Abstract

The present study was performed to clarify the relationship between human T cell lymphotropic virus type I (HTLV-I) infection and chronic inflammatory arthropathy. To determine the ability of HTLV-I to infect synovial cells and the effect on synovial cell proliferation, synovial cells were cocultured with the HTLV-I-producing T cell lines (MT-2 or HCT-1). After coculture with HTLV-I-infected T cells, the synovial cells expressed HTLV-I-specific core antigens, and HTLV-I proviral DNA was detected from the synovial cells by polymerase chain reaction. These cocultured synovial cells with HTLV-I-infected T cells proliferated more actively than the synovial cells cocultured with uninfected T cells. This stimulatory effect of HTLV-I-infected T cells on synovial cell proliferation seems necessary to contact each other. After being cocultured with MT-2 cells, synovial cells proliferated more actively than control cells even after several passages. Furthermore, HTLV-I-infected synovial cells produced significant amounts of granulocyte/macrophage colony-stimulating factor. These results suggest that HTLV-I can infect synovial cells, resulting their active proliferation and may be involved in the pathogenesis of proliferative synovitis similar to that found in rheumatoid arthritis.

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