Abstract:
:A major function of innate immune receptors is to recognize pathogen-associated molecular patterns and then evoke immune responses appropriate to the nature of the invading pathogen(s). Because innate immune cells express various types of these receptors, distinct combinations of signaling pathways are activated in response to a given pathogen. Although the conventional wisdom is that these signaling pathways cooperate with one another to ensure an effective host response, a more nuanced view recognizes antagonism between the individual pathways, where the attenuation of a signaling pathway(s) by others may shape the immune response. In this study, we show that, on Listeria monocytogenes infection, Toll-like receptor-triggered MyD88 signaling pathways suppress type I IFN gene induction, which is detrimental to macrophage bactericidal activity. These pathways target and suppress the IFN regulatory factor 3 (IRF3) transcription factor that is activated by the stimulator of IFN genes-TANK-binding kinase-1 kinase pathway. We also provide evidence for the involvement of the MAPK phosphatase family members, which renders IRF3 hypophosphorylated on Toll-like receptor signaling by enhancing the formation of an MAPK phosphatase-IRF3-TANK-binding kinase-1 ternary complex. This study, therefore, reveals a hitherto unrecognized and important contribution of a beneficial innate signaling interference against bacterial infections.
journal_name
Proc Natl Acad Sci U S Aauthors
Negishi H,Matsuki K,Endo N,Sarashina H,Miki S,Matsuda A,Fukazawa K,Taguchi-Atarashi N,Ikushima H,Yanai H,Nishio J,Honda K,Fujioka Y,Ohba Y,Noda T,Taniguchi S,Nishida E,Zhang Y,Chi H,Flavell RA,Taniguchi Tdoi
10.1073/pnas.1320145110subject
Has Abstractpub_date
2013-12-03 00:00:00pages
19884-9issue
49eissn
0027-8424issn
1091-6490pii
1320145110journal_volume
110pub_type
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