| First Author | Constant SL | Year | 2000 |
| Journal | J Immunol | Volume | 165 |
| Issue | 5 | Pages | 2671-6 |
| PubMed ID | 10946297 | Mgi Jnum | J:64050 |
| Mgi Id | MGI:1888636 | Doi | 10.4049/jimmunol.165.5.2671 |
| Citation | Constant SL, et al. (2000) JNK1 is required for T cell-mediated immunity against Leishmania major infection. J Immunol 165(5):2671-6 |
| abstractText | 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. |
