Response to 'Plasma proteins present in osteoarthritic synovial fluid can stimulate cytokine production via Toll-like receptor 4' - authors' reply
- † Equal contributors
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
Citation and License
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 2012First 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].
