Spondyloarthropathy: disease at the crossroads of immunity.
Up until recently, the prevailing paradigm relating to spondyloarthropathy (SpA) pathogenesis was that they were human leukocyte antigen (HLA)-associated, T-cell-driven autoimmune diseases. This view is now being questioned. Careful studies of well-characterised cohorts of patients with SpA, including detailed analysis of involved tissue, together with clinical trials of targeted treatments, in particular anti-tumour necrosis factor (TNF) therapies, have contributed enormously to both interest in and understanding of disease pathogenesis. In this chapter, our current knowledge and understanding of the relative contributions of the components of the innate and adaptive arms of the immune response to SpA pathogenesis is reviewed. It is clear that both arms of the immune response are involved and inter-dependent in SpA. With continued emphasis on discovery research, including detailed analysis of novel therapeutic interventions, significant additional breakthroughs in SpA are likely to be forthcoming.
FitzGerald
Oliver
O
St. Vincent's University Hospital, Elm Park, Dublin, 4, Ireland. ofitzger@iol.ie
McInnes
Iain
I
D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate; D007375:Interleukin-1 / Q000276:immunology; D015846:Monokines / Q000276:immunology; D010950:Plasma Cells / Q000276:immunology; D011565:Psoriasis / Q000188:drug therapy / Q000276:immunology; D025242:Spondylarthropathies / Q000188:drug therapy / Q000276:immunology*; D013582:Synovial Fluid / Q000276:immunology; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
D007375:Interleukin-1; D015846:Monokines; D014409:Tumor Necrosis Factor-alpha