Skip to main content


Different molecules at the surface of stimulated T cells induce IL-1beta, tumour necrosis factor and IL-1RA in human monocytes

Article metrics

  • 662 Accesses

Imbalance in cytokine homeostasis is thought to play an important part in the pathogenesis of chronic inflammatory diseases such as rheumatoid arthritis. We demonstrated that T cells might exert a pathological effect through direct cellular contact with monocyte-macrophages, inducing a massive upregulation of IL-1β and tumour necrosis factor (TNF) [1]. We showed that this mechanism that might be relevant to chronic inflammation is specifically inhibited by high-density lipoproteins (HDL) [2]. Like many other stimuli, besides proinflammatory cytokines, the contact-mediated activation of monocytes induces the production of cytokine inhibitors such as IL-1Ra. HDL inhibited the production of IL-1β and TNF but not that of IL-1Ra induced in monocytes activated by membranes isolated from stimulated T cells to mimic cellular contact. This was also the case in peripheral blood mononuclear cells stimulated by either phytoheamagglutinin or tetanus toxoid. Similarly, IL-1Ra mRNA expression was not inhibited contrary to IL-1β and TNF mRNA. This demonstrates that different molecules at the surface of stimulated HUT-78 cells are involved in the induction of IL-1β, TNF and IL-1Ra in monocytes, IL-1β and TNF being activated by HDL-specific ligand(s). Separation of CHAPS-solubilized membrane molecules by liquid isoelectric focusing showed that two activity peaks were present; one activating IL-1β, TNF and IL-1Ra production, the other inducing the production of IL-1Ra in the absence of IL-1β and TNF. Further isolation of these two types of factor by gel filtration demonstrated that factor(s) inducing IL-1β, TNF and IL-1Ra displayed a Mr around 40,000 kDa, whereas factors inducing IL-1Ra only displayed Mr around 70,000 kDa and 30,000 kDa. Thus different factors are expressed at the surface of stimulated T cells that differentially trigger the production of proinflammatory and anti-inflammatory factors, and are differently affected by HDL.


  1. 1.

    Burger D, Roux-Lombard P, Chizzolini C, Dayer JM: Cell–cell contact in chronic inflammation: the importance to cytokine regulation in tissue destruction and repair. Cytokines and Joint Injury. Edited by: van den Berg WB, Miossec P Basel. 2004, Birkhäuser Verlag, 165-188. [Parnham MJ (Series Editor): Progress in Inflammation Research.]

  2. 2.

    Hyka N, Dayer JM, Modoux C, Kohno T, Edwards CK, Roux-Lombard P, Burger D: Apolipoprotein A-I inhibits the production of interleukin-1beta and tumor necrosis factor-alpha by blocking contact-mediated activation of monocytes by T lymphocytes. Blood. 2001, 97: 2381-2389. 10.1182/blood.V97.8.2381.

Download references

Author information

Rights and permissions

Reprints and Permissions

About this article


  • Rheumatoid Arthritis
  • Tumour Necrosis Factor
  • Peripheral Blood Mononuclear Cell
  • Tetanus
  • Human Monocyte