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Spondyloarthritis encompasses a group of common inflammatory diseases caused by an overactive immune response affecting up to half a million people in the UK alone.

Spa synovium
Model for role of GM-CSF in spondyloarthritis chronic inflammation. GM-CSF is produced by joint-resident innate lymphoid cell (ILC) and infiltrating CD4 T cells and acts to activate monocytes to produce other molecules that propagate the inflammatory response.

In collaboration with the Wellcome Trust Centre for Human Genetic, NDORMS researchers have been working to establish the type of disease-causing immune cells in this condition in order to identify new treatments. Spondyloarthritis encompasses a group of common inflammatory diseases thought to be driven by IL-17A-secreting type-17 lymphocytes.

In a recent article published in Nature Communications the researchers identified the expansion of a subset of immune cells in patient blood and joint fluid that are likely to be driving the inflammation by releasing a particular inflammatory molecule called GM-CSF.  Both GM-CSF+ and IL-17A  cells express increased levels of GPR65, a proton-sensing receptor associated with spondyloarthritis. Silencing GPR65 in primary CD4 T cells reduces GM-CSF production. GM-CSF and GPR65 may thus serve as targets for therapeutic intervention of spondyloarthritis.

Commenting on the findings, lead researcher Dr Hussein Al-Mossawi says: “It is hoped that this research will inform new trials that target GM-CSF in order to treat patients who suffer from this disease.”

Read the full article on Nature Communications:

 The research is funded by the Wellcome Trust and the National Institute for Health Research (NIHR).