Journal
JOURNAL OF IMMUNOLOGY
Volume 165, Issue 5, Pages 2671-2676Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.165.5.2671
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- NIAID NIH HHS [AI-39158] Funding Source: Medline
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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, mere 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.
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