JNK and p38 MAP kinases in CD4+ and CD8+ T cells

Immunol Rev. 2003 Apr:192:131-42. doi: 10.1034/j.1600-065x.2003.00019.x.

Abstract

The c-Jun aminoterminal kinase (JNK) and p38 mitogen-activated protein (MAP) kinase signaling pathways have been associated with cell death, differentiation and proliferation. CD4+ and CD8+ T cells have different effector functions after antigen stimulation and control specific aspects of the immune response. The studies carried out in our group indicate that the role of JNK and p38 MAP kinases in CD4+ T cells is different from their role in CD8+ T cells. Moreover, these two pathways are not redundant in either T cell population. We have also shown that p38 MAP kinase regulates early stages of T cell development in the thymus. It is therefore important to consider the specific function of these kinases in each T cell population when pharmacological inhibitors of JNK and p38 MAP kinases are used for therapeutic purposes to control the immune response.

Publication types

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

MeSH terms

  • Animals
  • CD4-Positive T-Lymphocytes / enzymology*
  • CD4-Positive T-Lymphocytes / immunology
  • CD8-Positive T-Lymphocytes / enzymology*
  • CD8-Positive T-Lymphocytes / immunology
  • Cell Lineage
  • Interferon-gamma / metabolism
  • Interleukins / metabolism
  • JNK Mitogen-Activated Protein Kinases
  • Lymphocyte Activation
  • MAP Kinase Signaling System
  • Mice
  • Mitogen-Activated Protein Kinases / metabolism*
  • Models, Immunological
  • p38 Mitogen-Activated Protein Kinases

Substances

  • Interleukins
  • Interferon-gamma
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases