Protein kinase C is required for responses to T cell receptor ligands but not to interleukin-2 in T cells

Cell. 1988 Oct 7;55(1):101-12. doi: 10.1016/0092-8674(88)90013-x.


We have tested the role of protein kinase C in mRNA expression and T cell proliferation mediated through the T cell receptor and through the interleukin-2 (IL-2) receptor. Chronic treatment of a mouse T cell clone with phorbol esters caused a complete loss of protein kinase C activity and a concomitant loss of proliferation to T cell receptor ligands (antigen, lectins, antireceptor antibodies). In contrast, kinase C-depleted T cells retained the ability to proliferate to IL-2. Loss of the T cell receptor response was not due to decreased cell surface expression of receptor or impairment of early receptor function (phosphatidylinositol turnover, calcium mobilization). Kinase C-depleted T cells showed no induction of mRNAs for activation-associated genes on exposure to the T cell receptor ligand Concanavalin A; expression of a subset of the same mRNAs in response to IL-2 was unaffected. We conclude that kinase C is required for mRNA expression and subsequent proliferation mediated through the T cell receptor pathway but is not involved in mRNA expression and proliferation in response to IL-2.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cell Division / drug effects
  • Clone Cells
  • Interleukin-2 / pharmacology*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Phorbol Esters / pharmacology
  • Protein Kinase C / metabolism*
  • Receptors, Antigen, T-Cell / metabolism*
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / enzymology*


  • Interleukin-2
  • Phorbol Esters
  • Receptors, Antigen, T-Cell
  • Protein Kinase C