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

UMMS Affiliation

Graduate School of Biomedical Sciences; Program in Molecular Medicine

Publication Date


Document Type



Life Sciences | Medicine and Health Sciences


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.

DOI of Published Version



J Immunol. 2000 Sep 1;165(5):2671-6.

Journal/Book/Conference Title

Journal of immunology (Baltimore, Md. : 1950)

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Link to article in PubMed

PubMed ID