Abstract
We are pleased to read that our paper (Sutton et al., 2009), as well as that of Martin et al. (2009), has stimulated a debate on the importance of γδ T cells in interleukin-17 (IL-17) production and the signals that may drive this production. We acknowledge the contribution that O'Brien and colleagues have made to our understanding of the role of IL-17 production by γδ T cells in autoimmunity in our manuscript. However, we do not agree with their assertion that we “claim priority” or that we did not acknowledge previous contributions to the discovery that “γδ T cells can produce IL-17 without deliberate stimulation via the T cell receptor.” Indeed we cited the contribution by Shibata et al.
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