The active metabolite of spleen tyrosine kinase inhibitor fostamatinib abrogates the T cell priming capacity of dendritic cells

Andrew Platt, Ross McQueenie, Robert Benson, John Butcher, Martin Braddock, James M. Brewer, Iain B. McInnes, Paul Garside

Research output: Contribution to conferenceAbstract

Abstract

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.
Original languageEnglish
PagesS304
Number of pages1
DOIs
Publication statusPublished - Oct 2013

    Fingerprint

Keywords

  • Spleen tyrosine kinase, fostamatinib, T cell, dendritic cells

Cite this