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Science 21 October 1988:
Vol. 242. no. 4877, pp. 426 - 430
DOI: 10.1126/science.3262925
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Articles

Science, Vol 242, Issue 4877, 426-430
Copyright © 1988 by American Association for the Advancement of Science

articles

Kaposi's sarcoma cells: long-term culture with growth factor from retrovirus-infected CD4+ T cells

S Nakamura, SZ Salahuddin, P Biberfeld, B Ensoli, PD Markham, F Wong-Staal, and RC Gallo

Laboratory of Tumor Cell Biology, National Cancer Institute, Bethesda, MD 20892.

Studies of the biology and pathogenesis of Kaposi's sarcoma (KS) have been hampered by the inability to maintain long-term cultures of KS cells in vitro. In this study AIDS-KS-derived cells with characteristic spindle-like morphology were cultured with a growth factor (or factors) released by CD4+ T lymphocytes infected with human T-lymphotropic virus type I or II (HTLV-I or HTLV-II) or with human immunodeficiency virus type 1 or 2 (HIV-1 or HIV-2). Medium conditioned by HTLV-II-infected, transformed lines of T cells (HTLV-II CM) contained large amounts of this growth activity and also supported the temporary growth of normal vascular endothelial cells, but not fibroblasts. Interleukin-1 and tumor necrosis factor-alpha stimulated the growth of the KS-derived cells, but the growth was only transient and these could be distinguished from that in HTLV-II CM. Other known endothelial cell growth promoting factors, such as acidic and basic fibroblast growth factors and epidermal growth factor, did not support the long-term growth of the AIDS-KS cells. The factor released by CD4+ T cells infected with human retroviruses should prove useful in studies of the pathogenesis of KS.


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Risk Factors for Kaposi's Sarcoma in Patients With Advanced Human Immunodeficiency Virus Disease Treated With Zidovudine.
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HIV-Related Tumors of the Oral Cavity.
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Identification of a major growth factor for AIDS-Kaposi's sarcoma cells as oncostatin M.
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AIDS-Kaposi's sarcoma-derived cells express cytokines with autocrine and paracrine growth effects.
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Science. ISSN 0036-8075 (print), 1095-9203 (online)