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The Journal of Immunology, 2005, 174: 7393-7397.
Copyright © 2005 by The American Association of Immunologists

Cross Talk between MyD88 and Focal Adhesion Kinase Pathways1

Mirjam B. Zeisel2,*, Vanessa A. Druet2,*, Jean Sibilia{dagger}, Jean-Paul Klein*, Valérie Quesniaux3,{ddagger} and Dominique Wachsmann3,4,*

* Institut National de la Santé et de la Recherche Médicale 392, Faculté de Pharmacie, Illkirch, France; {dagger} Service de Rhumatologie, Hôpitaux Universitaires, Strasbourg, France; and {ddagger} Immunologie et Embryologie Moléculaires 2815, Transgenose Institute, Centre National de la Recherche Scientifique, Orleans, France

Focal adhesion kinase (FAK) is a nonreceptor protein tyrosine kinase involved in signaling downstream of integrins, linking bacterial detection, cell entry, and initiation of proinflammatory response through MAPKs and NF-{kappa}B activation. In this study, using protein I/II from Streptococcus mutans as a model activator of FAK, we investigated the potential link between FAK and TLR pathways. Using macrophages from TLR- or MyD88-deficient mice, we report that MyD88 plays a major role in FAK-dependent protein I/II-induced cytokine release. However, response to protein I/II stimulation was independent of TLR4, TLR2, and TLR6. The data suggest that there is a cross talk between FAK and MyD88 signaling pathways. Moreover, MyD88-dependent, LPS-induced IL-6 secretion by human and murine fibroblasts required the presence of FAK, confirming that MyD88 and FAK pathways are interlinked.




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