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Inflammatory Diseases Research, DuPont Merck Pharmaceutical Company, Wilmington, DE 19880
Three mitogen-activated protein kinase pathways are up-regulated during the activation of T lymphocytes, the extracellular signal-regulated kinase (ERK), Jun NH2-terminal kinase, and p38 mitogen-activated protein kinase pathways. To examine the effects of blocking the ERK pathway on T cell activation, we used the inhibitor U0126, which has been shown to specifically block mitogen-activated protein kinase/ERK kinase (MEK), the kinase upstream of ERK. This compound inhibited T cell proliferation in response to antigenic stimulation or cross-linked anti-CD3 plus anti-CD28 Abs, but had no effect on IL-2-induced proliferation. The block in T cell proliferation was mediated by down-regulating IL-2 mRNA levels. Blocking Ag-induced proliferation by inhibiting MEK did not induce anergy, unlike treatments that block entry into the cell cycle following antigenic stimulation. Surprisingly, induction of anergy in T cells exposed to TCR cross-linking in the absence of costimulation was also not affected by blocking MEK, unlike cyclosporin A treatment that blocks anergy induction. These results suggest that inhibition of MEK prevents T cell proliferation in the short term, but does not cause any long-term effects on either T cell activation or induction of anergy. These findings may help determine the viability of using mitogen-activated protein kinase inhibitors as immune suppressants.
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M. Saxena, S. Williams, J. Brockdorff, J. Gilman, and T. Mustelin Inhibition of T Cell Signaling by Mitogen-activated Protein Kinase-targeted Hematopoietic Tyrosine Phosphatase (HePTP) J. Biol. Chem., April 23, 1999; 274(17): 11693 - 11700. [Abstract] [Full Text] [PDF]
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S. J. Kempiak, T. S. Hiura, and A. E. Nel The Jun Kinase Cascade Is Responsible for Activating the CD28 Response Element of the IL-2 Promoter: Proof of Cross-Talk with the I{kappa}B Kinase Cascade J. Immunol., March 15, 1999; 162(6): 3176 - 3187. [Abstract] [Full Text] [PDF]
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A. M. Domina, J. H. Smith, and R. W. Craig Myeloid Cell Leukemia 1 Is Phosphorylated through Two Distinct Pathways, One Associated with Extracellular Signal-regulated Kinase Activation and the Other with G2/M Accumulation or Protein Phosphatase 1/2A Inhibition J. Biol. Chem., July 7, 2000; 275(28): 21688 - 21694. [Abstract] [Full Text] [PDF]
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K. M. F. Khan, D. J. Falcone, and R. Kraemer Nerve Growth Factor Activation of Erk-1 and Erk-2 Induces Matrix Metalloproteinase-9 Expression in Vascular Smooth Muscle Cells J. Biol. Chem., January 11, 2002; 277(3): 2353 - 2359. [Abstract] [Full Text] [PDF]
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S. Namura, K. Iihara, S. Takami, I. Nagata, H. Kikuchi, K. Matsushita, M. A. Moskowitz, J. V. Bonventre, and A. Alessandrini Intravenous administration of MEK inhibitor U0126 affords brain protection against forebrain ischemia and focal cerebral ischemia PNAS, September 25, 2001; 98(20): 11569 - 11574. [Abstract] [Full Text] [PDF]
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