Why does chronic inflammatory joint disease persist?
Inflammation is a beneficial host response to tissue damage. Most episodes of inflammation resolve spontaneously and do not persist. However, in rheumatoid arthritis (RA), as in a number of other chronic inflammatory diseases, the inflammatory response persists and a stable inflammatory infiltrate accumulates in the joint. What drives this persistence and the relative contribution of infiltrating leucocytes and stromal cells such as fibroblasts to the stability of the inflammatory process are the subject of this article. Fibroblasts play an important role in defining the disordered synovial microenvironment in RA. Through their production of a variety of cytokines and constitutive chemokines they directly alter the behaviour of infiltrating leucocytes, leading to their inappropriate survival and retention. These findings suggest that stromal cells such as fibroblasts play an important role in the switch from acute resolving to chronic persistent arthritis by allowing lymphocytes to accumulate in the wrong place at the wrong time.
Buckley
Christopher D
CD
Department of Rheumatology, City Hospital NHS Trust, University of Birmingham.
D001168:Arthritis / Q000276:immunology* / Q000378:metabolism; D018925:Chemokines / Q000096:biosynthesis; D005347:Fibroblasts / Q000276:immunology / Q000378:metabolism; D006801:Humans; D017154:Stromal Cells / Q000276:immunology / Q000378:metabolism; D013583:Synovial Membrane / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism
D018925:Chemokines