Ubiquitination of Innate Immune Regulator TRAF3 Orchestrates Expulsion of Intracellular Bacteria by Exocyst Complex.
Immunity
; 45(1): 94-105, 2016 07 19.
Article
en En
| MEDLINE
| ID: mdl-27438768
ABSTRACT
Although the intracellular trafficking system is integral to most physiologic activities, its role in mediating immune responses to infection has remained elusive. Here, we report that infected bladder epithelial cells (BECs) mobilized the exocyst complex, a powerful exporter of subcellular vesicles, to rapidly expel intracellular bacteria back for clearance. Toll-like receptor (TLR) 4 signals emanating from bacteria-containing vesicles (BCVs) were found to trigger K33-linked polyubiquitination of TRAF3 at Lys168, which was then detected by RalGDS, a guanine nucleotide exchange factor (GEF) that precipitated the assembly of the exocyst complex. Although this distinct modification of TRAF3 served to connect innate immune signaling to the cellular trafficking apparatus, it crucially ensured temporal and spatial accuracy in determining which among the many subcellular vesicles was recognized and selected for expulsion in response to innate immune signaling.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Infecciones Urinarias
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Vejiga Urinaria
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Urotelio
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Vesículas Transportadoras
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Factor 3 Asociado a Receptor de TNF
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Escherichia coli
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Inmunidad Innata
Límite:
Animals
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Female
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Humans
Idioma:
En
Año:
2016
Tipo del documento:
Article