Distinctive calcineurin-dependent (FK506-sensitive) mechanisms regulate the production of the CC chemokines macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, and RANTES vs IL-2 and TNF-alpha by activated human T cells

Cell Immunol. 1998 Dec 15;190(2):121-31. doi: 10.1006/cimm.1998.1411.

Abstract

Calcineurin (CaN) controls the production of multiple cytokines, including IL-2 and TNF-alpha, during T cell activation. However, its role in chemokine production is unclear. Here, we used the CaN inhibitor FK506 to probe for the contribution of CaN in MIP-1alpha, MIP-1beta, and RANTES production at the protein and mRNA levels in human T cells stimulated via CD3/PMA or CD3/CD28. With both modes of activation, FK506 inhibited RANTES production only partially and late during a 3-day culture, whereas it suppressed both MIP-1alpha and MIP-1beta production throughout the culture. However, FK506 inhibition was more pronounced on MIP-1beta than MIP-1alpha, especially in CD3/CD28-activated T cells. Surprisingly, FK506 also significantly reduced MIP-1beta induction by PMA alone. Furthermore, comparison with IL-2 and TNF-alpha revealed that both were more potently inhibited by the drug upon CD3/PMA or CD3/CD28 induction than either MIP-1alpha or MIP-1beta. These differences in FK506 sensitivity were also observed in CD4(+) and CD8(+) T cell subsets. Therefore, all three chemokines are affected by FK506 distinctly from one another and from IL-2 and TNF-alpha, suggesting that CaN participates to different extents in the induction of these cytokines during T cell activation. Further evidence that this induction relies on distinctive mechanisms, depending on the cytokine, came from analyses of the kinetics and cycloheximide sensitivity of cytokine mRNA expression.

MeSH terms

  • CD28 Antigens / metabolism
  • CD3 Complex / metabolism
  • Calcineurin / physiology*
  • Calcineurin Inhibitors
  • Cells, Cultured
  • Chemokine CCL3
  • Chemokine CCL4
  • Chemokine CCL5 / biosynthesis
  • Chemokine CCL5 / genetics
  • Cycloheximide / pharmacology
  • Cytokines / biosynthesis*
  • Cytokines / genetics
  • Dose-Response Relationship, Drug
  • Gene Expression
  • Humans
  • Interferon-gamma / biosynthesis
  • Interleukin-2 / biosynthesis
  • Lymphocyte Activation*
  • Macrophage Inflammatory Proteins / biosynthesis
  • Macrophage Inflammatory Proteins / genetics
  • Mitogens / metabolism
  • Mitogens / pharmacology
  • Protein Synthesis Inhibitors / pharmacology
  • RNA, Messenger
  • T-Lymphocyte Subsets / drug effects
  • T-Lymphocyte Subsets / metabolism
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / metabolism
  • Tacrolimus / pharmacology
  • Tetradecanoylphorbol Acetate / metabolism
  • Tetradecanoylphorbol Acetate / pharmacology
  • Time Factors
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • CD28 Antigens
  • CD3 Complex
  • Calcineurin Inhibitors
  • Chemokine CCL3
  • Chemokine CCL4
  • Chemokine CCL5
  • Cytokines
  • Interleukin-2
  • Macrophage Inflammatory Proteins
  • Mitogens
  • Protein Synthesis Inhibitors
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma
  • Cycloheximide
  • Calcineurin
  • Tetradecanoylphorbol Acetate
  • Tacrolimus