Human Th1 cells preferentially induce interleukin (IL)-1beta while Th2 cells induce IL-1 receptor antagonist production upon cell/cell contact with monocytes

Eur J Immunol. 1997 Jan;27(1):171-7. doi: 10.1002/eji.1830270125.


The role of human T cells in the induction and regulation, upon cell/cell contact, of inflammatory responses by monocytic cells was investigated. The production of interleukin (IL)-1beta and IL-1 receptor antagonist (IL-1Ra) by the monocytic THP-1 cell line was measured upon contact with either Th1 or Th2 cell clones. CD4+ T cell clones specific for purified protein derivative of Mycobacterium tuberculosis, predominantly Th1 [high interferon (IFN)-gamma and low IL-4 producers], or tetanus toxoid, predominantly Th2 (low IFN-gamma and high IL-4 producers), were generated. Cell membranes from antigen-stimulated, but not from resting T cell clones induced dose-dependent cytokine production by THP-1 cells. Th1 clones induced higher levels of IL-1beta production (484-806 pg/ml) than did Th2 clones (21-114 pg/ml). In contrast, Th1 clones induced lower levels of IL-IRa (0.9-7.8 ng/ml) than did Th2 clones (7.0-49.6 ng/ml). Similar results were obtained when T cell clones were activated by cross-linked CD3 and CD28. IL-1beta production by THP-1 cells correlated with IFN-gamma production by T cell clones but was unaffected by IFN-gamma neutralization. IL-1Ra production by THP-1 cells correlated with IL-4 production by T cells and was partially inhibited by IL-4 neutralization. These data indicate that activated Th1 and Th2 cells express different molecules on the cell surface able to induce distinct pro-inflammatory (IL-1beta) or anti-inflammatory (IL-1Ra) responses in monocytes. This differential induction of molecules with opposite effects on inflammation stresses the functional heterogeneity in CD4+ T cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD28 Antigens / physiology
  • CD3 Complex / physiology
  • Cell Adhesion
  • Cell Communication
  • Cell Division
  • Cells, Cultured
  • Humans
  • Inflammation / physiopathology*
  • Interferon-gamma / biosynthesis
  • Interleukin 1 Receptor Antagonist Protein
  • Interleukin-1 / biosynthesis*
  • Interleukin-4 / biosynthesis
  • Lymphocyte Activation
  • Monocytes / immunology*
  • Sialoglycoproteins / biosynthesis*
  • Signal Transduction
  • Th1 Cells / immunology*
  • Th2 Cells / immunology*


  • CD28 Antigens
  • CD3 Complex
  • IL1RN protein, human
  • Interleukin 1 Receptor Antagonist Protein
  • Interleukin-1
  • Sialoglycoproteins
  • Interleukin-4
  • Interferon-gamma