Research

My research is in the pathogenesis of inflammatory joint disease, especially ankylosing spondylitis and related diseases. I am interested in how genes associated with these diseases, especially HLA-B27, influence susceptibility to disease by affecting immune responses. In particular the lab works on a form of  arthritis  related to ankylosing spondylitis, reactive arthritis, triggered by bacterial infection, including Chlamydia trachomatis. We examine in detail the interaction between host and bacteria and its possible role in arthritis

Current work in the laboratory  is examining factors which affect production of the cytokine IL-23, particularly the role of ER stress, since IL-23 drives IL-17 production, which appears central to joint inflammation in these diseases.

Selected References

Evans, D.M., Spencer, C.C., Pointon, J.J.,  et al. Interaction between ERAP1 and HLA-B27 in ankylosing spondylitis implicates peptide handling in the mechanism for HLA-B27 in disease susceptibility. Nat. Genet. 43: 761-767 (2011).

Prevosto, C., Goodall, J.C. and Gaston, J.S.H. Cytokine secretion by Pathogen Recognition Receptor-stimulated dendritic cells in rheumatoid arthritis and ankylosing spondylitis. J. Rheumatol.  39: 1918-28 (2012).

Gaston, J.S.H., Goodall, J.C. and Baeten, D.L.M. IL-23: a central cytokine in spondyloarthritis pathogenesis. Arthrits Rheum. In press (2011).

Goodall, J.C., Wu, C., Zhang, Y., Ellis, L., O’Brien, L., Saudek, V. and Gaston, J.S.H.  ER stress signals are integrated by dendritic cells to enhance IL-23 responses to Toll-like receptor.  PNAS (USA) [direct submission] 107: (41) 17698-17703 (2010).

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