Background/Purpose: Spleen tyrosine kinase (SYK) is a core signaling protein that drives inflammatory responses and is fundamental to the propagation of signals via numerous immune-receptors including the B cell receptor (BCR) and Fc receptors (FcRs). The small molecule SYK inhibitor, fostamatinib, has shown evidence of ameliorating inflammation in rheumatoid arthritis (RA) patients. We sought to understand how the active metabolite of fostamatinib, R406, affects the inflammatory response at the cellular level. It has been shown that R406 reduces the response of dendritic cells (DCs) to immune complexes (ICs) and we have previously demonstrated that the area and duration of interaction between T cells and DCs are key determinants in the outcome of an immune response.
|Number of pages||1|
|Publication status||Published - Oct 2013|
- Spleen tyrosine kinase, fostamatinib, T cell, dendritic cells
Platt, A., McQueenie, R., Benson, R., Butcher, J., Braddock, M., Brewer, J. M., McInnes, I. B., & Garside, P. (2013). The active metabolite of spleen tyrosine kinase inhibitor fostamatinib abrogates the T cell priming capacity of dendritic cells. S304. https://doi.org/10.1002/art.38216