Letter

Response to 'Plasma proteins present in osteoarthritic synovial fluid can stimulate cytokine production via Toll-like receptor 4' - authors' reply

Dong Hyun Sohn12, Jeremy Sokolove12, Orr Sharpe12, Jennifer C Erhart34, Piyanka E Chandra12, Lauren J Lahey12, Tamsin M Lindstrom12, Inyong Hwang12, Katherine A Boyer34, Thomas P Andriacchi34 and William H Robinson12*

Author Affiliations

1 GRECC, VA Palo Alto Health Care System, MC 154R, 3801 Miranda Avenue Palo Alto, CA 94304, USA

2 Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA

3 Bone and Joint Center, VA Palo Alto Health Care System, 3801 Miranda Avenue, Palo Alto, CA 94304, USA

4 Department of Mechanical Engineering, Stanford University, Stanford, CA 94305, USA

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Arthritis Research & Therapy 2012, 14:406  doi:10.1186/ar3892


See related research by Sohn et al., http://arthritis-research.com/content/14/1/R7, and related letter by Oliviero et al., http://arthritis-research.com/content/14/5/405

Published: 12 September 2012

First paragraph (this article has no abstract)

We thank Oliviero and colleagues for their interest in our recent publication [1] and for reporting their very interesting related experiments [2]. Their results strongly support the concept that extravascular plasma proteins may act as damage-associated molecular patterns, and specifically as Toll-like receptor 4 agonists. In addition, we note that the NALP-3 inflammasome exhibits dependence on Toll-like receptor 4 or other mechanisms of priming of IL-1β transcription, thereby generating pro-IL-1β that can be converted to IL-1β by the activated inflammasome [3].