The Chronically Infected Promonocytic Cell Line U1: A Model of HIV Expression Regulated by Cytokines

Retinoic acid mimics transforming growth factor beta in the regulation of human immunodeficiency virus expression in monocytic cells.

“…4). Furthermore, we have extended these observations to the primary MDM system, despite the fact that a significant variability exists in the susceptibility to HIV infection in cultures established from different seronegative donors (23,40). Pretreatment with TGF-18 or RA resulted in increased expression of HIV in cultures that showed poor ability to support HIV replication in the absence of these factors (Fig.…”

“…2B), as described in TGF-j3-treated cells (23). No significantly enhanced transcription of viral RNA was observed in U1 cells stimulated with either IL-6 or GM-CSF even when cells were synergistically stimulated with glucocorticoids, although significant levels of HIV proteins and particles were produced [a phenomenon that we referred to as posttranscriptional induction (40)]. Therefore, no RNA studies were performed on RA-or TGF-f-treated cells under these stimulatory conditions.…”

“…described (23,40). RA or TGF-,3 were added to part of the cultures before and throughout the entire culture period after infection (pretreatment protocol), whereas other cultures were incubated with the cytokines only 7-10 days after infection and throughout the subsequent culture period (posttreatment protocol).…”

Characterization of an Antagonist Interleukin-6 Dimer by Stable Isotope Labeling, Cross-linking, and Mass Spectrometry

“…Abnormal IL-6 production is associated with a variety of diseases (2) such as rheumatoid arthritis (3), AIDS (4,5), osteoporosis (6,7), psoriasis (8), multiple myeloma (9, 10) and Kaposi's sarcoma (11). Thus the interactions between IL-6 and its associated receptors, the transmembrane glycoproteins IL-6R and gp130 (12), present an attractive target for therapeutic antagonists (13).…”

The designer cytokine hyper-IL-6 mediates growth inhibition and GM–CSF-dependent rejection of B16 melanoma cells

“…It acts as a di erentiation factor for T-and B-cells and promotes the expansion of early haematopoietic stem cells (Akira et al, 1993). Altered IL-6 serum levels have been reported for several diseases, including plasmacytoma (Suematsu et al, 1992), rheumatoid arthritis (Hermann et al, 1989), Castleman's Disease (Brandt et al, 1990) and AIDS (Poli et al, 1990). Furthermore, it has been shown in mice that levels of endogenous IL-6 paralleled with tumor burden indicating an important role of IL-6 in the host's immune responses to cancer (McIntosh et al, 1989).…”