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. The interaction between the immune system and microbial agents, both pathogens and commensals, in the pathogenesis of spondyloarthritis is also a major focus of interest. Current work in the laboratory is examining factors which affect production of the cytokines IL-23 and TSLP, particularly the role of ER stress, since IL-23 drives IL-17 production, which appears central to joint inflammation in these diseases. Our research uses blood and joint fluid or tissue from patients and healthy controls, and we employ a wide range of biochemical and immunologic techniques.
Goodall JC, Wu C, Zhang Y, Ellis L, O’Brien L, Saudek V and Gaston JSH. (2010) 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
Gaston JSH, Goodall JC and Baeten DLM. (2011) IL-23: a central cytokine in spondyloarthritis pathogenesis. Arthrits Rheum. 63:3668-71
Prevosto C, Goodall JC and Gaston JSH. (2013) Cytokine secretion by Pathogen Recognition Receptor-stimulated dendritic cells in rheumatoid arthritis and ankylosing spondylitis. J. Rheumatol. 39:1918-28
Benham H, Norris PG, Goodall JC, Wechalekar M, Szentpetery A, FitzGerald O, Smith MD, Thomas R Gaston JSH. (2014) Th22 and Th17 cells in psoriatic arthritis and psoriasis.
Arthritis Research & Therapy 15: R136 doi:10.1186/ar4317
Wu C, Goodall JC, Busch R and Gaston JSH. (2015) Relationship of CD146 expression to secretion of interleukin (IL)-17, IL-22 and interferon-γ by CD4+ T cells in patients with inflammatory arthritis. Clin Exp Immunol doi:10.1111/cei.12434 In press
Areas of expertise
Immunology, T lymphocyte, Cytokine biology, Spondyloarthritis, Reactive arthritis, Chlamydia trachomatis