A defect in the protein kinase C system in T cells from patients with systemic lupus erythematosus

Clin Immunol Immunopathol. 1991 Aug;60(2):220-31. doi: 10.1016/0090-1229(91)90065-i.


To determine whether there is an intrinsic defect in T cells from patients with systemic lupus erythematosus (SLE), we studied signal transduction systems, assaying the total protein kinase C (PKC) levels and the phorbol myristate acetate (PMA)-induced activation of PKC in PHA-treated T cells. T cells from SLE patients showed a decrease in proliferation in response to PMA, but not to PHA, thereby suggesting the existence of an intrinsic abnormality in the PKC-mediated activation pathway. Total PKC activity in the T cells from SLE patients was significantly decreased. Although stimulation with PMA induced a translocation of PKC from the cytosol to the particulate fraction, translocated PKC activity after 2 nM PMA treatment was decreased in the SLE T cells. Furthermore, PMA-induced phosphorylation of 80-kDa substrates was also decreased in SLE T cells. These results suggest that there is a reduced PKC activity and an impaired PKC activation in response to PMA in the SLE T cells, a finding which may explain, if partially, the defect in T cell activation in patients with SLE.

MeSH terms

  • Biological Transport, Active
  • Cell Division
  • Cells, Cultured
  • Cytosol / chemistry
  • Female
  • Humans
  • In Vitro Techniques
  • Lupus Erythematosus, Systemic / enzymology*
  • Lymphocyte Activation / physiology
  • Male
  • Phosphorylation
  • Phytohemagglutinins / pharmacology
  • Protein Kinase C / metabolism*
  • Signal Transduction
  • T-Lymphocytes / enzymology*
  • Tetradecanoylphorbol Acetate / pharmacology


  • Phytohemagglutinins
  • Protein Kinase C
  • Tetradecanoylphorbol Acetate