Effects of soluble interleukin‐1 receptor and tumor‐necrosis factor receptor, respectively, on the IL‐1‐ and TNF‐α‐induced DNA synthesis of acute myeloblastic leukemia blasts in vitro

Abstract

This study demonstrates that soluble interleukin‐1 receptor and tumor necrosis factor receptor modulate their corresponding cytokine‐induced DNA synthesis of acute myeloblastic leukemia (AML) blasts in a dose‐dependent, bimodal fashion; at lower concentrations they enhanced, while at high concentrations they inhibited, the cytokine‐mediated effects. Furthermore, the concentrations of endogenously produced IL‐1β and TNF‐a were found to be significantly (p<0.01) higher in supernatants of AML cells cultured in the presence of corresponding soluble receptors compared to their levels in supernatants of cells growing in the absence of these molecules. Our data might suggest that the attenuation of the spontaneous decay of IL‐1β as well as TNF‐a activities by soluble receptors may account for their ability to augment some of their effects.

Th1 cytokines in pediatric acute lymphoblastic leukemia

“…In ALL, TNF-α has been reported to exert either proliferative or cytotoxic effects on primary blast cells ex vivo [ 8 ]. TNFR-1 mainly induces apoptotic signaling by engaging a death domain (e.g., in bacterial response), whereas TNFR-2 predominantly regulates survival signaling (e.g., in immune cell activation) [ 9 ].…”

Proinflammatory Cytokine-Receptor Interaction Model Improves the Predictability of Cerebral White Matter Injury in Preterm Infants

“…Some of these endogenous control systems have facilitative effects on the bioactivity of their corresponding cytokine, whereas others are inhibitory. [14][15][16] Modeling the interaction of proinflammatory cytokines with their soluble receptors might provide a better estimate of cytokine bioactivity and a more complete picture of in vivo inflammatory events. In this pilot study we hoped to develop more fully the idea of modeling cytokine and soluble cytokine-receptor interaction in plasma obtained from a cohort of high-risk premature infants.…”