JNK1 is required for T cell-mediated immunity against Leishmania major infection

J Immunol. 2000 Sep 1;165(5):2671-6. doi: 10.4049/jimmunol.165.5.2671.

Abstract

c-Jun N-terminal kinase (JNK) is a mitogen-activated protein kinase that plays important regulatory roles in helper T cell differentiation. In the current study, we used Jnk1-deficient mice to examine the function of JNK during an in vivo pathogenic infection, leishmaniasis, which is strongly influenced by Th1/Th2 effector mechanisms. The data show that Jnk1-deficient mice, despite their usually genetically resistant background, were unable to resolve Leishmania infections. Jnk1-/- mice displayed reduced delayed-type hypersensitivity in response to the pathogen, which was associated with a T cell defect. We found that, although these mice can direct an apparent Th1-response, there is also simultaneous generation of Leishmania-specific Th2 responses, which possibly down-modulate protective Th1-mediated immune function. These findings demonstrate that the negative regulation of Th2 cytokine production by the JNK1 signaling pathway is essential for generating Th1-polarized immunity against intracellular pathogens, such as Leishmania major.

Publication types

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

MeSH terms

  • Animals
  • CD4-Positive T-Lymphocytes / cytology
  • CD4-Positive T-Lymphocytes / enzymology
  • CD4-Positive T-Lymphocytes / immunology
  • CD4-Positive T-Lymphocytes / parasitology
  • Cell Differentiation / genetics
  • Cell Differentiation / immunology
  • Cytokines / biosynthesis
  • Cytokines / physiology
  • Hypersensitivity, Delayed / genetics
  • Hypersensitivity, Delayed / immunology
  • Hypersensitivity, Delayed / parasitology
  • Immunity, Cellular / genetics
  • Leishmania major / immunology*
  • Leishmaniasis, Cutaneous / enzymology*
  • Leishmaniasis, Cutaneous / genetics
  • Leishmaniasis, Cutaneous / immunology*
  • Lymphocyte Activation / genetics
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mitogen-Activated Protein Kinase 8
  • Mitogen-Activated Protein Kinases / deficiency
  • Mitogen-Activated Protein Kinases / genetics
  • Mitogen-Activated Protein Kinases / physiology*
  • T-Lymphocyte Subsets / cytology
  • T-Lymphocyte Subsets / enzymology*
  • T-Lymphocyte Subsets / immunology*
  • T-Lymphocyte Subsets / parasitology
  • Th1 Cells / cytology
  • Th1 Cells / enzymology
  • Th1 Cells / immunology
  • Th1 Cells / parasitology
  • Th2 Cells / cytology
  • Th2 Cells / enzymology
  • Th2 Cells / immunology
  • Th2 Cells / parasitology

Substances

  • Cytokines
  • Mitogen-Activated Protein Kinase 8
  • Mitogen-Activated Protein Kinases