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Review: Ubiquitination and de-ubiquitination: role in regulation of signaling by Toll-like receptors

Division of Pediatric Infectious Diseases and Immunology, the Burns and Allen Research Institute, Cedars-Sinai Medical Center and David Geffen School of Medicine at UCLA, Los Angeles, California USA

Terence M. Doherty

Division of Pediatric Infectious Diseases and Immunology, the Burns and Allen Research Institute, Cedars-Sinai Medical Center and David Geffen School of Medicine at UCLA, Los Angeles, California USA

Hisae Karahashi

Division of Pediatric Infectious Diseases and Immunology, the Burns and Allen Research Institute, Cedars-Sinai Medical Center and David Geffen School of Medicine at UCLA, Los Angeles, California USA

Moshe Arditi

Division of Pediatric Infectious Diseases and Immunology, the Burns and Allen Research Institute, Cedars-Sinai Medical Center and David Geffen School of Medicine at UCLA, Los Angeles, California USA, moshe.arditi{at}cshs.org

Signaling by Toll-like receptors (TLRs) has attracted accelerating attention over the past decade because of the central role of TLR signaling in both innate and adaptive immunity. In addition, TLR signaling is now increasingly implicated in a remarkably wide range of diseases that are either caused, or accompanied, by dysregulated inflammation. Much has been learned about the basic signaling framework and participants, as well as how signaling is turned off and fine-tuned. Here, we summarize key aspects of TLR signaling, focusing on interaction with the anti-inflammatory TGF-ß signaling network. We propose that ubiquitination and de-ubiquitination of TLR pathway components may be a mechanism by which predominantly anti-inflammatory input is integrated into the host response to fine-tune inflammation in accordance with the needs of host defenses.

Key Words: De-ubiquitination • inflammation • innate immunity • Toll-like receptor • ubiquitin

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