TNF-alpha and IL-1beta cross-desensitization of astrocytes and astrocytoma cell lines

J Neuroimmunol. 1998 Jul 1;87(1-2):17-26. doi: 10.1016/s0165-5728(98)00041-1.

Abstract

Exposure of human astrocytes and astrocytoma cell lines to TNF-alpha, IL-1beta and gammaIFN induce expression of a specific member of the intercrine/chemokine family of cytokines, RANTES. Pre-incubation with non-stimulatory concentrations of TNF-alpha inhibit IL-1beta-stimulated RANTES expression and similarly, non-stimulatory concentrations of IL-1beta inhibits TNF-alpha induced RANTES expression. The lowered responsiveness of these cells is stably maintained for at least 24 h. The inhibitory effect of TNF-alpha on IL-1beta-induced responses was mediated by TNF receptor-1 since low concentrations of a specific anti-TNF receptor-1 antiserum mimicked the inhibitory effect. These results indicate that TNF and IL-1 receptors mediate pro- and antiinflammatory responses in a concentration dependent manner, suggesting that at low receptor occupancy, TNF and IL-1 receptors may share a common signaling pathway and behave as endogenous antiinflammatory cytokines.

MeSH terms

  • Astrocytes / drug effects*
  • Astrocytoma / pathology*
  • Cell Line / drug effects
  • Chemokine CCL5 / antagonists & inhibitors
  • Dose-Response Relationship, Drug
  • Humans
  • Interferon-gamma / pharmacology
  • Interleukin-1 / pharmacology*
  • Interleukin-6 / metabolism
  • Osmolar Concentration
  • Receptors, Tumor Necrosis Factor / physiology
  • Substrate Specificity
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Chemokine CCL5
  • Interleukin-1
  • Interleukin-6
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma