UMMS Affiliation

Program in Molecular Medicine

Date

1-1-2008

Document Type

Article

Disciplines

Biochemistry | Cell Biology | Cellular and Molecular Physiology | Immunity | Immunology of Infectious Disease | Molecular Biology

Abstract

Gamma interferon (IFN-gamma) plays a critical role in the early eradication of Anaplasma phagocytophilum. However, the mechanisms that regulate IFN-gamma production upon infection remain poorly understood. Here we show that c-Jun NH2-terminal kinase 2 (JNK2) inhibits IFN-gamma production during A. phagocytophilum infection. jnk2-null mice were more refractory to infection with A. phagocytophilum and produced increased levels of IFN-gamma after challenge with the pathogen. The resistance of jnk2-null mice to A. phagocytophilum infection was due to elevated levels of IFN-gamma secreted by conventional and natural killer (NK) T cells. The administration of alpha-galactosylceramide, a strong NK T-cell agonist, increased IFN-gamma release and protected mice from A. phagocytophilum, further demonstrating the inhibitory effect of JNK2 on IFN-gamma production. Collectively, these findings provide strong evidence that JNK2 is an important regulatory protein for IFN-gamma secretion upon challenge with A. phagocytophilum.

Rights and Permissions

Citation: Infect Immun. 2008 Jan;76(1):308-16. Epub 2007 Nov 12. Link to article on publisher's site

Publisher PDF posted as allowed by the publisher's author rights policy at http://journals.asm.org/site/misc/ASM_Author_Statement.xhtml.

Related Resources

Link to Article in PubMed

Keywords

Gamma interferon, Anaplasma phagocytophilum infection, c-Jun NH2-terminal kinase 2 (JNK2)

PubMed ID

17998313

 
 

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