Abstract:
:Adaptive immune responses by dendritic cells (DCs) are critically controlled by Toll-like receptor (TLR) function. Little is known about modulation of TLR-specific signaling by other pathogen receptors. Here, we have identified a molecular signaling pathway induced by the C-type lectin DC-SIGN that modulates TLR signaling at the level of the transcription factor NF-kappaB. We demonstrated that pathogens trigger DC-SIGN on human DCs to activate the serine and threonine kinase Raf-1, which subsequently leads to acetylation of the NF-kappaB subunit p65, but only after TLR-induced activation of NF-kappaB. Acetylation of p65 both prolonged and increased IL10 transcription to enhance anti-inflammatory cytokine responses. We demonstrated that different pathogens such as Mycobacterium tuberculosis, M. leprae, Candida albicans, measles virus, and human immunodeficiency virus-1 interacted with DC-SIGN to activate the Raf-1-acetylation-dependent signaling pathway to modulate signaling by different TLRs. Thus, this pathway is involved in regulation of adaptive immunity by DCs to bacterial, fungal, and viral pathogens.
journal_name
Immunityjournal_title
Immunityauthors
Gringhuis SI,den Dunnen J,Litjens M,van Het Hof B,van Kooyk Y,Geijtenbeek TBdoi
10.1016/j.immuni.2007.03.012subject
Has Abstractpub_date
2007-05-01 00:00:00pages
605-16issue
5eissn
1074-7613issn
1097-4180pii
S1074-7613(07)00219-1journal_volume
26pub_type
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