Important note: Information in this article was accurate in 1997. The state of the art may have changed since the publication date.
The possible role of soluble IL-6R in growth of AIDS-Kaposi's sarcoma cells (Meeting abstract).
Proc Annu Meet Am Assoc Cancer Res; 38:A791 1997. Unique Identifier : AIDSLINE MED/97622044 Murakami-Mori K; Mori S; Taga T; Kishimoto T; Nakamura S; Huntington Memorial Hospital, Pasadena, CA 91105
Abstract:
Kaposi's sarcoma (KS) is most frequently associated with HIV-infected individuals. We found that the soluble IL-6R binding subunit (sIL-6Ralpha) functions as a potent growth factor for AIDS-KS cells, while IL-6 alone has no effect on KS cell growth. KS cells express considerable amounts of the signal transducing subunit (gp130) of IL-6R, but only a scanty amount of IL-6Ralpha. This phenotype can account for the lack of IL-6 responsiveness of KS cells and its acquisition by addition of sIL-6Ralpha. Since KS cells express high levels of IL-6, it is likely that, in the presence of sIL-6Ralpha, these cells acquire an IL-6 autocrine growth loop. Anti-gp130 antibodies blocked the action of sL-6Ralpha on KS cells, hence, we refer to sIL-6Ralpha as a gp130-related KS cell growth factor. Increased levels of sIL-6Ralpha as well as IL-6 have been noted in the sera of HIV-infected patients. Therefore, perturbed production of sIL-6Ralpha may play a crucial role in development of KS by directly acting on KS cell growth. Clinical observations indicate that glucocorticoid therapy is a possible risk factor in KS. We noted that dexamethasone (Dex), in a synergistic manner, enhances the gp130-mediated KS cell growth, while Dex alone slightly augments the basal growth. We also report evidence for existence of specific interaction in KS cells between glucocorticoid and the gp130-related growth factors.
Keywords: *Acquired Immunodeficiency Syndrome/METABOLISM *Antigens, CD/METABOLISM *Interleukin-6/METABOLISM *Receptors, Interleukin/METABOLISM *Sarcoma, Kaposi/METABOLISM 971230
M97C1599
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