Fascinating concept and hypothesis. treating AS and not going after the cytokines.
Could we imagine trying to target a specific
pathogenic IL-17-producing cell population – for
example, using imatinib to deplete c-kit-positive mast
cells and innate lymphoid cells – rather than the cytokines they produce in order to leave the protective IL-17
production untouched ? It is mainly in the context of
selective therapeutic targeting that the work of Appel and
colleagues set a first, but crucial, step in characterisation
of the phenotype, developmental and transcriptional
requirements, and function of innate IL-17-producing
cells in SpA.
Source: (it is a PDF)http://www.biomedcentral.com/content/pdf/ar3351.pdf