JNK1 is required for T cell-mediated immunity against Leishmania major infection
Authors
Constant, Stephanie L.Dong, Chen
Yang, Derek D.
Wysk, Mark Allen
Davis, Roger J.
Flavell, Richard A.
Document Type
Journal ArticlePublication Date
2000-08-18Keywords
Animals; CD4-Positive T-Lymphocytes; Cell Differentiation; Cytokines; Hypersensitivity, Delayed; Immunity, Cellular; Leishmania major; Leishmaniasis, Cutaneous; Lymphocyte Activation; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Knockout; Mitogen-Activated Protein Kinase 8; Mitogen-Activated Protein Kinases; T-Lymphocyte Subsets; Th1 Cells; Th2 CellsLife Sciences
Medicine and Health Sciences
Metadata
Show full item recordAbstract
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.Source
J Immunol. 2000 Sep 1;165(5):2671-6.
DOI
10.4049/jimmunol.165.5.2671Permanent Link to this Item
http://hdl.handle.net/20.500.14038/33574PubMed ID
10946297Related Resources
ae974a485f413a2113503eed53cd6c53
10.4049/jimmunol.165.5.2671