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Janus Kinase-STAT Signaling and Gene Induction by Down-Regulation of the IFN- Receptor1
Departments of
*
Medical Microbiology and Immunology and
Microbiology, Ohio State University, Columbus, OH 43210
Macrophage activation is required to control the growth of
intracellular pathogens. Recent data indicate that macrophages become
functionally deactivated during mycobacterial infection. We studied
macrophage deactivation by examining the expression of a panel of
IFN-
-inducible genes and activation of Janus Kinase (JAK)-STAT
pathway in Mycobacterium avium-infected macrophages.
Reduced expression of IFN--inducible genes—MHC class II gene Eß;
MHC class II transactivator; IFN regulatory factor-1; and Mg21, a gene
coding for a GTP-binding protein—was observed in M.
avium-infected macrophages. Decreased tyrosine phosphorylation
and DNA binding activity of STAT1 in M. avium-infected
macrophages stimulated with IFN- was observed. Tyrosine
phosphorylation of JAK1, JAK2, and IFN-R
was also reduced in
infected cells. Northern and Western blot analyses showed that a
down-regulation of IFN-R - and ß-chain mRNA and protein
occurred in M. avium-infected macrophages. The
down-regulation of IFN-R and inhibition of STAT1 activation were
time dependent and required 4 h of infection for down-regulation
of the IFN-R and 8 h for STAT1 inhibition. These findings
suggest that M. avium infection inhibits induction of
IFN--inducible genes in mouse macrophages by down-regulating
IFN-R, resulting in reduced phosphorylation of IFN-R, JAK1,
JAK2, and STAT1.
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