Second International Congress Drug Therapy in HIV Infection 18-22 November 1994 Glasgow, UK

THE ROLE OF CYTOKINES AND CYTOKINE INHIBITORS IN AIDS-RELATED KAPOSI'S SARCOMA,

Mitsuyasu R.T., Miles S.A.
Center for Clinical AIDS Research and Education (CARE), University of California, Los Angeles, BH-412 Center for the Health Sciences, Los Angeles, California 90024-1793, U.S.A.

Int Cong Drug Therapy HIV 1994 Nov 18-22;2:Abstract No. 13.5
AIDS 1994, Vol. 8 (Suppl. 4);S11

Kaposi's sarcoma (KS) is a multi-focal tumor of uncertain origin that is frequently associated with HIV infection. The tumor is seen in other immunodeficiency states, and in HIV infection its growth is often accelerated at the time of opportunistic infection or progression of HIV disease. Recent advances in our understanding of the pathogenesis of Kaposi's sarcoma through the use of in vitro KS cell lines have shown that these tumors produce several autocrine and paracrine growth factors and respond to a variety of known cytokines and the HIV-tat protein. Factors such as IL-1β, IL-6, BFGF, TNF-α and oncostatin-m have potent stimulatory effects on Kaposi's sarcoma cells in vitro. Several of these cytokines are believed to act through increasing IL-6 production or effect its receptors on KS cells. Intervention with agents that.inhibit the elaboration of these growth factors such as IL-4, platelet factor-4, pentoxifylline, vesnarinone and other agent may slow or reverse the growth of Kaposi's sarcoma cells. Agents which directly compete with the receptor of KS inducing growth factors such as sTNFr and sIL-1r may also inhibit KS cell growth. Transforming growth factor beta (TGF-β) and γ-interferon have complex effects on KS cell growth in vitro perhaps through biphasic effects on known KS growth factors such as IL-6. Several cytokine regulators or competitive inhibitors are now in early clinical trials in patients with Kaposi's sarcoma. These studies may help answer important questions on the pathogenesis of this unusual tumor in patients with HIV as well as provide potentially more effective means of treating or preventing this tumor.

Presenting author: Mitsuyasu R.T.

1994-11-18
13.5

Originally published in AIDS Volume 8, Supplement 4 and hosted with permission of the publisher Lippincott Williams & Wilkins, 250 Waterloo Road, London, SE1 8RD, UK. Tel: +44 (0)20 7981 0700 Fax: +44 (0) 7981 0701

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